384 


THE  LIBRARY 

OF 

THE  UNIVERSITY 
OF  CALIFORNIA 

LOS  ANGELES 


GIFT  OF 

SAN  FRANCISCO 
COUNTY  MEDICAL  SOCIETY 


"  WITH  all  our  varied  instruments  of  precision,  useful  as  they 
are,  nothing  can  replace  the  watchful  eye,  the  alert  ear,  the  tactful 
finger,  and  the  logical  mind  which  correlates  the  facts  obtained 
through  all  these  avenues  of  information  and  so  reaches  an  exact 
diagnosis." 

W.   W.   KEEN. 


4284 
PRINCIPLES  AND  PRACTICE 


OF 


PHYSICAL   DIAGNOSIS 


BY 

JOHN    C.  DACOSTA,  JR.,  M.  D. 

ASSOCIATE    PROFESSOR  OF  MEDICINE,    JEFFERSON    MEDICAL    COLLEGE;    ASSISTANT    VISITING 

PHYSICIAN,    JEFFERSON   HOSPITAL;  HEMATOLOGIST,    GERMAN  HOSPITAL;   CONSULTING 

PHYSICIAN,    NORTHWESTERN   GENERAL  HOSPITAL;   FELLOW  OF  THE  COLLEGE 

OF    PHYSICIANS    OF    PHILADELPHIA;     FELLOW    OF    THE     AMERICAN 

ACADEMY   OF   MEDICINE,    ETC. 


WITH  243  OFUGINAL  ILLUSTRATIONS 


THIRD  EDITION,  THOROUGHLY  REVISED 


PHILADELPHIA  AND  LONDON 

W.    B.    SAUNDERS   COMPANY 

1915 


Copyright,   1908,   by  W.  B.  Saunders   Company.     Reprinted  June,  1909,  and 

September,  1910.     Revised,  reprinted,  and  recopy righted  September, 

1911.     Reprinted  August,  1913.     Revised,  reprinted, 

and   recopyrighted   November,    1915 


Copyright,  1915,  by  W.  B.  Saunders  Company 


PKINTCO     IN     AMCMICA 


Jiomedieal 
Library 


TO  THE  MEMORY  OF 
MY  UNCLE 

JOHN   MEIGS,   Ph.  D. 

HEAD  MASTER  OF  THE  HILL  SCHOOL 


624180 


PREFACE  TO  THE  THIRD  EDITION 


BY  selective  deletion  and  recasting  of  the  text  it  has  been 
possible  to  keep  the  size  of  this  new  edition  within  bounds  and 
to  preserve  the  original  character  of  the  previous  printings, 
despite  the  addition  of  considerable  new  matter  chiefly  dealing 
with  technical  methods,  and  with  diseases  of  the  lungs,  the 
heart,  and  the  stomach.  To  keep  abreast  of  the  recent  ad- 
vances in  physical  diagnosis  the  subjects  of  vertebral  per- 
cussion, sphygmomanometry,  electrocardiography,  and  gastric 
radiography  receive  due  attention;  mediastinal  pleurisy,  the 
lobar  type  of  bronchopneumonia,  and  the  acute  pulmonary 
edema  of  chlorin  gassing  are  described;  and  auricular  fibrilla- 
tion, auricular  flutter,  ventricular  fibrillation,  and  the  various 
cardiac  arhythmias  are  discussed  from  a  clinical  standpoint. 

The  author  is  indebted  to  Dr.  W.  F.  Manges  for  several 
new  radiographic  plates;  to  Dr.  T.  A.  Cope  and  Dr.  E.  B. 
Krumbhaar  for  a  number  of  original  electrocardiograms;  and 
to  Mr.  J.  V.  Alteneder  for  the  other  illustrations.  To  his  pub- 
lishers appreciation  is  due  for  their  willingness  to  substitute 
new  printings  for  the  revision  called  for  two  years  ago  and 
unavoidably  delayed  until  the  present  time. 

PHILADELPHIA,  November,  1915. 


PREFACE 


THE  purpose  of  this  book  is  to  present,  within  reasonable  compass, 
the  principles  of  physical  diagnosis,  and  to  apply  this  means  of 
research  to  the  study  of  thoracic  and  abdominal  diseases?  To  meet 
the  requirements  of  junior  students,  especial  consideration  is  given 
to  clinical  anatomy  and  to  the  origin,  mechanism,  and  meaning  of 
normal  physical  signs;  while  in  order  to  guide  those  farther  advanced 
in  the  study  and  practice  of  medicine,  the  subjects  of  pathology  and 
diagnosis  are  accorded  commensurate  prominence.  Throughout, 
a  consistent  endeavor  is  made  to  keep  in  view  the  prime  impor- 
tance of  interpreting  morbid  objective  data,  individual  or  grouped, 
on  the  basis  'of  pathologic  cause  and  physical  effect,  and  to  analyze 
such  findings  in  the  light  of  a  full  clinical  inquiry.  In  the  section 
dealing  with  technic  the  theory  and  practice  of  the  simpler  direct 
methods  of  physical  examination  are  explained  in  detail,  and  also 
certain  instrumental  procedures  adapted  to  routine  bedside  inves- 
tigation. Useful  laboratory  information,  in  so  far  as  it  applies  to 
the  diagnosis  of  particular  lesions,  is  discussed  in  connection  there- 
with, but  an  account  of  special  laboratory  technic,  not  being  germane 
to  the  plan  of  this  work,  is  omitted. 

The  subject  matter  of  the  following  pages  is  based  primarily  upon 
the  author's  lecture-notes,  and  the  views  expressed  were  molded 
largely  by  ten  years'  clinical  and  teaching  experience  in  internal 
medicine  and  study  of  pathology,  aided  and  supplemented  by  much 
information  derived  from  acknowledged  authorities  and  from  con- 
tributions of  merit  found  in  text-books,  monographs,  and  periodical 
literature.  "  Information  gleaned  from  these  sources  has  been  duly 
accredited  in  the  text,  save  in  the  case  of  facts  that  by  time  and  usage 
have  become  a  matter  of  common  scientific  knowledge. 

5 


6  PREFACE 

Care  has  been  taken  to  secure  an  adequate  number  of  original 
illustrations  that  will  prove  helpful  to  the  reader,  those  representing 
various  clinical  conditions  having  been  reproduced  from  photographs 
of  patients  observed  in  the  Jefferson  Hospital  and  in  the  Philadelphia 
General  Hospital,  and  those  showing  pathologic  lesions  having  been 
made  from  Kaiserling  preparations  by  Dr.  R.  C.  Rosenberger  and 
Dr.  John  Funke,  of  the  pathological  staffs  of  these  institutions. 
Recknagel  model-studies  and  figures  standardized  to  Cunningham 
have  been  utilized  for  many  of  the  diagrams  by  Mr.  E.  F.  Faber 
and  by  Mr.  J.  V.  Alteneder.  The  sphygmograms  and  cardiograms 
are  the  work  of  Dr.  George  Bachmann,  and  the  radiographic  plates 
were  made  by  Dr.  W.  F.  Manges.  For  the  cooperation  so  cordially 
extended  by  these  gentlemen  hearty  thanks  are  herewith  returned. 

The  author  takes  pleasure  in  acknowledging  the  aid  rendered 
by  his  wife  in  lightening  the  task  of  proof- revision;  in  thanking 
Dr.  S.  A.  Munford  for  many  useful  criticisms  and  suggestions 
relating  to  technical  questions;  and  in  expressing  appreciation  of 
his  publishers'  numerous  courtesies  and  liberal  policies. 


CONTENTS 


SECTION   I 

PAOS 

METHODS  AND  TECHNIC  OF  PHYSICAL  EXAMINATION n 

Inspection 12 

Palpation 12 

Percussion 12 

Auscultation 22 

Thoracometry  and  Cyrtometry 29 

Sphygmomanometry 31 

Sphygmography  and  Cardiography 37 

Electrocardiography 43 

Paracentesis 47 

Fluoroscopy  and  Radiography 65 

The  Tuberculin  Reaction 67 

SECTION  II 

EXAMINATION  OF  THE  THORAX 70 

Clinical  Anatomy 70 

Normal  Landmarks 71 

Topographic  Lines  and  Areas 74 

Pathologic  Types 77 

Local  Asymmetry 86 

Respiratory  Movements 92 

Anomalies  of  Respiration 95 

Dyspnea 100 

Cyanosis 104 

Venous  Enlargement  and  Tortuosity 104 

Edema  of  the  Thoracic  Wall 106 

Glandular  Enlargement 109 

Pain  in  the  Thorax 117 

SECTION  III 

EXAMINATION  OF  THE  BRONCHOPULMONARY  SYSTEM I22 

Clinical  Anatomy 122 

Inspection 1*8 

Palpation 13° 

Percussion J35 

Auscultation  of  the  Lungs J51 

Respiratory  Sounds I52 

Vocal  Resonance J59 

Adventitious  Sounds IO° 

Splashing  Sounds l(>9 

7 


8  CONTENTS 

SECTION    IV  PACF. 

DlSKASKS  OF  THE  BRONCHOPULMOXARY  SYSTEM  AND  MEDIASTINUM I?! 

Acute  Catarrhal  Bronchitis 171 

Chronic  Catarrhal  Bronchitis 174 

Fibrinous  Bronchitis 175 

Bronchial  Asthma 177 

Bronchiectasis 179 

Bronchostenosis 183 

Pulmonary  Congestion 185 

Pulmonary  Edema 188 

Pulmonary  Hemorrhagic  Infarction IQO 

Catarrhal  Pneumonia 192 

Croupous  Pneumonia 198 

Chronic  Interstitial  Pneumonia 213 

Acute  Pneumonic  Phthisis 216 

Chronic  Ulcerative  Phthisis 220 

Fibroid  Phthisis 234 

Pulmonary  Syphilis 237 

Emphysema 240 

Hypertrophic 24 1 

Atrophic 246 

Compensatory 246 

Acute  Vesicular 247 

Interstitial 248 

Atelectasis 248 

Pneumonoconiosis 252 

Pulmonary  Abscess 255 

Pulmonary  Gangrene 257 

Pulmonary  Neoplasms 260 

Actinomycosis 264 

Echinococcus  Cyst 265 

Pleurisy 266 

Acute  Fibrinous 267 

Serofibrinous 268 

Purulent 278 

Circumscribed 281 

Chronic  Adhesive 283 

Hydrothorax 285 

Hemothorax 286 

Chylothorax 287 

Pneumothorax •. 287 

Pleural  Neoplasms 295 

Mediastinitis 296 

Mediastinal  Lymphadenitis 298 

Mediastinal  Neoplasms 301 

SECTION  V 

EXAMINATION  OF  THE  CARDIOVASCULAR  SYSTEM 308 

Clinical  Anatomy 308 

Mechanism  of  the  Circulation 31  * 

Inspection  and  Palpation 3*5 

Percussion 35° 

Auscultation 355 

Adventitious  Sounds 372 

Endocardial  Murmurs 372 

Exocardial  Sounds i 3&9 

Vascular  Murmurs. . .  392 


CONTENTS  9 

SECTION  VI  PAGE 

DISEASES  OF  THE  CARDIOVASCULAR  SYSTEM 396 

Pericarditis 396 

Acute  Fibrinous 396 

Serofibrinous 398 

Purulent * 401 

Chronic  Adhesive 402 

Hydropericardium 406 

Hemopericardium 406 

Pneumopericardium 405 

Cardiac  Hypertrophy 407 

Cardiac  Dilatation 4I4 

Myocarditis 417 

Acute  Endocarditis 421 

Chronic  Endocarditis 427 

Mitral  Regurgitation 434 

Mitral  Stenosis 439 

Aortic  Regurgitation 449 

Aortic  Stenosis 457 

Tricuspid  Regurgitation 462 

Trkuspid  Stenosis 465 

Pulmonary  Stenosis 467 

Pulmonary  Regurgitation 471 

Congenital  Cardiac  Disease 473 

Aneurism  of  the  Aorta 476 

Aneurism  of  Thoracic  Aorta 476 

Aneurism  of  Abdominal  Aorta 493 

SECTION  VII 

EXAMINATION  OF  THE  ABDOMEN  AND  THE  ABDOMINAL  VISCERA 495 

Clinical  Anatomy 495 

Topographic  Lines  and  Areas 498 

Methods  of  Abdominal  Examination 500 

Clinical  Types  of  Abdomen 503 

Local  Abdominal  Enlargements 5°9 

Abdominal  Movements 512 

The  Skin  and  Subcutaneous  Tissues 513 

Fluctuation 515 

Tactile  Friction  and  Thrills 5*6 

Pain  in  the  Abdomen S1^ 

Examination  of  the  Stomach 5J9 

Examination  of  the  Intestines S32 

Examination  of  the  Liver  and  Gall-bladder 539 

Examination  of  the  Pancreas 549 

Examination  of  the  Spleen 55° 

Examination  of  the  Kidneys 557 

INDEX 563 


PHYSICAL  DIAGNOSIS 


SECTION   I 

METHODS  AND  TECHNIC  OF  PHYSICAL 
EXAMINATION 


IN  the  common  acceptance  of  the  term,  physical  diagnosis  relates 
primarily  to  the  objective  study  of  disease  by  the  four  cardinal  methods 
of  inspection,  palpation,  percussion,  and  auscultation,  the  success- 
ful practice  of  which  depends  upon  the  intelligent  exercise  of  the 
examiner's  senses  of  sight,  feeling,  and  hearing.  In  suitable  instances 
certain  clinical  instruments  are  used  as  an  aid  and  a  supplement  to 
these  means  of  inquiry:  the  thermometer,  to  take  the  patient's  tem- 
perature; the  stethoscope,  to  facilitate  auscultation;  the  tape-measure, 
calipers,  and  cyrtometer,  to  determine  diameters,  circumferences, 
and  shapes;  the  exploring  needle,  to  obtain  specimens  of  body-fluids; 
and  the  tonometer,  the  sphygmograph,  and  the  electrocardio- 
graph, to  study  the  blood-pressure  and  other  details  of  the 
circulatory  system. 

In  addition  to  the  foregoing  methods  of  physical  diagnosis  the 
clinician  has  at  his  disposal  a  number  of  technical  procedures  that 
require  training  in  the  use  of  special  instruments  of  precision  and  in 
laboratory  technic,  and  upon  the  intimate  correlation  of  the  data 
derived  from  both  these  sources,  bedside  and  laboratory,  a  finished 
diagnosis  must  be  based.  Although,  in  a  broad  sense,  the  diagnostic 
application  of  the  Rontgen-ray  and  analyses  of  the  urine,  blood, 
sputum,  gastro-intestinal  contents,  and  body-fluids  belong  to  the 
subject  of  physical  diagnosis,  the  technic  and  principles  of  these  pro- 
cedures are  too  highly  specialized  to  receive  more  than  parenthetic 
reference  in  the  following  pages,  which  deal  purely  with  the  theory 
and  practice  of  physical  diagnosis  at  the  bedside,  with  reference  to 
the  study  of  thoracic  and  abdominal  lesions. 


12  PHYSICAL    DIAGNOSIS 

INSPECTION 

Inspection,  or  visual  examination  of  the  patient,  is  the  first,  and  in 
some  instances  the  all-important,  step  in  a  routine  physical  examina- 
tion. "We  make  more  mistakes  by  not  looking  than  by  not  know- 
ing "  is  an  aphorism  of  Edward  Jenner  that  every  beginner  in  the 
study  of  physical  diagnosis  should  take  as  a  maxim.  To  neglect 
or  to  gloss  over  careful  inspection  of  the  patient  deprives  one  of  a 
means  of  information  for  which  skill  in  percussion  or  in  ausculta- 
tion cannot  compensate. 

A  general  inspection  shows  the  individual's  appearance,  body  con- 
formation, and  gait;  the  approximate  height  and  weight;  the  con- 
dition of  the  muscular  and  adipose  structures;  and  the  marks  of 
various  cachexias  and  of  scarring  or  eruptive  diseases.  Inspection 
of  a  circumscribed  area,  with  the  patient's  clothing  removed,  may 
betray  at  a  glance  some  organic  lesion,  or  at  least  may  give  a  clue 
to  be  verified  by  other  procedures.  The  facies  of  pneumonia,  of 
phthisis,  and  of  Bright's  disease,  the  barrel  chest  of  emphysema, 
and  the  throbbing  tumor  of  aneurism  are  familiar  examples  of  dis- 
eases that  in  time  indelibly  stamp  their  subjects  with  visible  signs 
so  characteristic  as  immediately  to  direct  the  clinician  along  cor- 
rect lines  of  inquiry. 

PALPATION 

Palpation,  or  examination  by  means  of  the  tactile  sense  of  the  fingers 
and  the  palms  of  the  hands,  is  employed  in  studying  various  vibrations 
referable  to  the  bronchopulmonary  system  (fremitus),  to  the  cardio- 
vascular apparatus  (thrill),  and  to  the  serous  surfaces  (friction). 
The  palpating  hand  can  also  appreciate  the  wavy  impulse  of  pent-up 
fluid  agitated  by  striking  its  delimiting  parietes  (fluctuation),  and 
can  recognize  rhythmic  throbbing  of  cardiovascular  origin  (pulsa- 
tion). The  site,  size,  shape,  mobility,  resistance,  and  tenderness  of 
a  local  area  of  the  body  are  also  determined  principally  by  the  tactile 
sense  of  the  examiner's  hand. 

The  special  technic  of  inspection  and  palpation  in  the  examina- 
tion of  various  regions  and  organs  is  described  subsequently. 

PERCUSSION 

Percussion  is  the  act  of  striking  or  tapping  the  surface  of  the 
body  so  as  to  elicit  sounds  of  diagnostic  utility,  the  clinical  value 
of  this  method  depending  upon  the  fact  that  different  anatomic 
structures,  when  struck  by  the  finger-tips  or  with  a  suitable  instru- 
ment, give  rise  to  different  sounds,  the  acoustics  of  which  vary  accord- 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       13 


ing  to  the  physical  properties  of  the  parts  percussed.  Fundamen- 
tally, all  percussion-sounds  are  either  •  resonant  or  dull,  of  which 
essential  properties  there  are  several  modifications,  notably,  hyper- 
resonance,  tympany,  and  flatness,  together  with  several  other  special 
shades  of  sound  not  exactly  expressed  by  any  of  these  terms.  By 
noting  the  character  of  the  sounds  and  the  degree  of  resistance  over 
the  region  percussed,  one  is  able  to  judge  the  density  of  the  under- 
lying structures  and  to  delimit  the 
boundaries  of  parts  containing  dif- 
ferent volumes  of  air. 

The  percussion  blow  may  be 
struck  either  with  the  finger-tips 
(finger  percussion)  or  with  a  small 
hammer  (instrumental  percussion). 
By  the  method  known  as  mediate 
Percussion  the  sound  is  elicited  by 
laying  a  finger  (pleximeter  finger) 
flat  upon  the  part  and  tapping  it 
with  one  or  two  fingers  (plexor  fin- 
gers) of  the  other  hand;  or  a  small 
rubber  plate  may  be  used  as  a 
pleximeter  and  a  specially  devised 
percussion  hammer  as  a  plexor. 
In  the  practice  of  immediate  per- 
cussion, little  used  at  the  present 
time,  the  part  is  tapped  without  the 
intermediation  of  a  pleximeter. 

Percussion,  though  exploited  by  Auenbrugger  in  1761,  did  not 
come  into  general  use  until  half  a  century  later,  when,  in  1808, 
Corvisart's  researches,  prompted  largely  by  the  teachings  of  Stoll, 
crystallized  the  diverse  and  fantastic  theories  and  methods  of  per- 
cussion into  a  tangible,  concrete  means  of  clinical  inquiry.  Piorry 
and  Barry,  the  advocates  of  instrumental  percussion,  and  Skoda, 
who,  in  1839,  correlated  the  various  percussion-sounds  with  correct 
physical  factors,  were  conspicuous  figures  in  the  development  of 
Auenbrugger's  principle,  now  so  indispensable  to  diagnosis. 

Technic. — It  is  best  to  percuss  the  bare  surface  of  the  body,  though 
a  thin  covering  of  underclothing  does  not  materially  interfere.  Mus- 
cular relaxation,  natural  breathing,  and  an  unconstrained  posture, 
either  erect  or  prone,  as  the  circumstances  direct,  are  requisites  for 
the  best  results. 

In  performing  mediate  finger  percussion  (Fig.  i)   the  palmar 


Fig.  i. — Technic  of  mediate  percus- 
sion. 


14  PHYSICAL    DIAGNOSIS 

surface  of  the  middle  finger  of  the  left  hand  is  laid  upon  the  surface 
of  the  body  and  sharply  struck  with  the  tip  of  the  middle  finger  of 
the  right  hand,  the  plexor  finger  being  crooked  so  as  to  deliver  a  per- 
pendicular blow,  which  should  fall  upon  the  dorsal  surface  of  the 
pleximeter  finger  at  the  base  of  the  nail  or  at  the  middle  of  the  second 
phalanx.  Four  precautions  are  to  be  observed:  the  pleximeter  finger 
must  be  kept  in  firm,  close,  accurate  contact  with  the  surface  of  the 
body;  the  force  of  the  percussion  strokes  must  be  as  equal  as  possi- 
ble; the  blow  must  be  delivered  entirely  by  a  movement  of  the  wrist, 
with  the  elbow  rigid  and  immovable;  and  the  action  of  the  plexor 
finger  must  be  rapkl,  accurate,  and  rebounding.  The  force  of  the 
stroke  is  strong  or  light,  according  to  the  situation  of  the  organ  or 
lesion  percussed,  whether  deep  or  superficial.  (See  Fig.  77.)  Too 
forcible  percussion,  even  of  a  deep-seated  structure,  is  to  be  guarded 
against,  since  it  may  set  up  such  intense  vibrations  outside  of  the 
circumscribed  area  that  a  confusing  commingling  of  sounds  is  pro- 
duced. The  more  forcible  the  percussion-stroke,  the  firmer  should 
be  the  pressure  of  the  pleximeter  finger,  and  vice  versa.  The  plexi- 
meter finger  should  be  kept  parallel  to  the  outline  of  the  part  to 
be  delimited.  A  few  careful  strokes  will  demonstrate  the  character- 
istics of  the  sounds  and  of  the  resistance  much  better  than  a  long 
succession  of  blows.  Prolonged  percussion  dulls  one's  auditory  and 
tactile  perceptions,  just  as  long-continued  looking  at  the  two  tints  in 
a  hemoglobinometer  blunts  one's  color-sense. 

Goldscheider's  method  of  threshold  percussion  may  prove  use- 
ful in  outlining  the  cardiac  and  hepatic  borders,  the  technic  con- 
sisting of  tapping  lightly  with  the  finger  upon  a  glass  rod  pleximeter 
one  end  of  which,  fitted  with  a  rubber  cap,  rests  upon  an  intercostal 
space,  the  rod  meanwhile  being  held  at  an  angle  to  the  surface  of  the 
thorax  and  parallel  to  the  borders  of  the  organ  thus  to  be  delimited. 
This  method  of  percussion  possesses  the  advantage  of  confining  the 
percussion  vibrations  to  a  very  restricted  area,  and  affords  accurate 
data  at  the  hands  of  one  skilled  in  its  use. 

Immediate  percussion  is  performed  by  directly  striking  the  sur- 
face with  a  plexor  (finger  or  instrumental),  or  of  delivering  a  series 
of  sharp  slaps  with  the  flat  of  the  hand.  The  method  is  distinctly 
inferior  to  mediate  percussion,  owing  to  the  defective  sounds  pro- 
duced and  also  because  it  robs  the  examiner  of  definite  tactile  impres- 
sions, so  essential  in  judging  the  character  of  sounds.  Immediate 
percussion  is  employed  chiefly  in  demonstrating  extensive  areas  of 
dulness  and  tympany,  in  eliciting  the  cardiac  and  the  pulmonary 
reflexes,  and  in  the  practice  of  auscultatory  percussion  (q.  v.  i.) . 


METHODS   AND  TECHNIC   OF   PHYSICAL  EXAMINATION       15 

Palpatory  percussion  is  a  combination  of  palpation  and  percus- 
sion affording  tactile  rather  than  auditory  impressions,  which  are 
elicited  by  gently  striking  the  pleximeter  finger  with  the  pads  of  the 
plexor  fingers,  the  latter  being  kept  almost  straight,  so  as  to  produce 
more  of  a  pushing  impact  than  a  perpendicular  blow,  this  peculiarity 
being  the  more  emphasized  by  continuing  the  plexor-pleximeter 
pressure  for  a  few  moments  after  the  stroke.  Rebounding  piano- 
hammer  strokes  are  to  be  avoided,  and  the  arc  of  the  percussion 
push  should  not  exceed  one  or  two  inches  (2.5  to  5  cm.). 
Although  perhaps  a  superior  method  of  examination  for  those 


Fig.  2. — Technic  of  auscultatory  percussion. 

skilled  in  its  technic,  palpatory  percussion  is  in  no  sense  a  substi- 
tute for  ordinary  mediate  percussion  in  routine  work. 

Auscultatory  Percussion. — Auscultatory  or  stethoscopic  per- 
cussion is  the  act  of  listening  to  the  percussion-sounds  with  a  stetho- 
scope applied  to  the  part  under  examination,  instead  of  directly 
judging  the  sound  in  the  ordinary  manner.  It  is  adapted  especially 
to  outlining  various  solid  and  hollow  organs,  such  as  the  heart,  the 
liver,  the  spleen,  the  stomach,  and  the  colon;  in  determining  the 
limits  of  effusions  and  consolidations;  and  in  circumscribing  cavities 
and  tumors.  By  auscultatory  percussion  of  a  superficial  echinococ- 
cus  cyst  it  is  sometimes  possible  to  distinguish  a  deep,  sonorous 
sound  of  hydatid  resonance. 


i6 


PHYSICAL    DIAGNOSIS 


In  auscultatory  percussion  the  chest-piece  of  a  binaural  stetho- 
scope is  placed  over  the  part  to  be  delimited,1  where  it  is  held  in 
position  by  the  patient  or  by  an  assistant,  while  the  examiner,  listening 
through  the  instrument,  begins  to  percuss  very  gently  at  several 
points  encircling  the  organ  and  well  beyond  its  outer  boundary 
(Fig.  2).  Continuing  the  percussion  toward  the  organ,  along  con- 
verging lines  centering  at  the  chest-piece  of  the  stethoscope,  the 
sounds  become  distinctly  louder  and  altered  in  pitch  and  in  quality 
when  the  periphery  of  the  organ  is  reached.  A  line  joining  these 


\ 


Fig.  3. — Illustrating  the  technic  of  auscultatory  percussion:   a-b,  Percussion  lines; 
b,  points  of  acoustic  change;  c,  chest-piece  of  stethoscope. 

several  points  of  acoustic  change  corresponds  to  the  limits  of  the 
organ  in  question  (Fig.  3). 

Several  modifications  of  this,  the  usual,  technic  of  auscultatory 
percussion  also  enjoy  more  or  less  vogue,  and  perhaps  merit  con- 
fidence. Thus,  the  sound  may  be  produced  by  direct  stroking  of 
the  surface  with  the  finger-tips,  instead  of  by  actual  percussion — 
stroke  auscultation;  by  rubbing  the  fingers  up  and  down,  a  grooved 
wooden  stick  applied  perpendicularly  to  the  surface — rod  ausculta- 
tion (Reichmann);  or  by  tapping  with  one  forefinger  the  second 

1  Le  Fevre  prefers  to  auscultate  the  percussion-sounds  with  the  chest-piece  of 
the  stethoscope  held  just  above  the  point  of  percussion,  but  not  touching  the 
surface,  in  order  to  eliminate  the  vibrations  of  the  bony  thorax. 


METHODS    AND    TECHNIC    OF    PHYSICAL   EXAMINATION        17 

joint  of  the  other  forefinger  applied  perpendicularly  to  the  part — 
Kordnyi's  method.  The  substitution  of  a  vibrating  tuning-fork  for 
the  plexor  finger  has  been  suggested  (Warder),  the  examiner  noting 
the  changes  in  the  intensity  and  quality  of  the  musical  vibrations  as 
the  fork  passes  over  the  surface  toward  the  part  under  investi- 
gation. 

Attributes  of  the  Percussion-sound. — Four  different  acoustic 
properties,  quality,  pitch,  duration,  and  intensity,  are  to  be  recognized 
as  clinically  important  attributes  of  the  percussion-sound.  Since 
verbal  description  can  convey  but  an  inadequate  idea  of  these  funda- 
mental sound  elements,  each  one  must  be  studied  practically  by  the 
student  in  order  to  appreciate  their  individual  peculiarities.  Their 
every-day  application  will  be  understood  when  they  are  referred  to 
later,  in  connection  with  the  questions  of  resonance,  dulness,  and 
other  phases  of  the  percussion-sound.  The  resistance  offered  to  the 
pleximeter  (or  percussed)  finger  is  also  of  the  greatest  utility  in  deter- 
mining the  nature  of  the  region  examined. 

By  the  term  quality  is  meant  that  essential  element  by  which  the 
particular  source  of  a  given  sound  is  distinguished,  whether  it  be  a 
vocal,  an  instrumental,  or  other  tone.  Thus,  this  quality,  timber,  or 
tone-color  enables  one  instantly  to  discriminate  between  a  masculine 
and  a  feminine  voice,  between  the  sounds  of  a  bass-drum  and  a  snare- 
drum,  and  between  the  tones  of  a  fife  and  an  oboe,  a  piano  and  an 
organ,  and  other  musical  instruments.  Physically,  the  quality  of 
sounds  is  determined  by  the  type  of  vibrations  by  which  they  are 
generated,  the  more  complex  vibrations  giving  rise  to  sounds  of  greater 
individuality  than  those  of  simpler  character.  It  is  this  element  of 
quality,  then,  that  is  the  clue  to  the  origin  and  nature  of  different 
sounds,  which  cannot  be  judged  by  criteria  such  as  pitch,  intensity, 
and  duration. 

The  pitch  of  a  sound  is  an  acoustic  attribute  thoroughly  appreci- 
able only  by  those  who  are  gifted  with  a  "musical  ear."  It  was 
Austin  Flint  who  first  called  attention,  in  1852,  to  the  value  of 
pitch  variations  in  the  acoustics  of  percussion  and  respiratory 
sounds.  Variations  in  pitch  are  governed  by  the  rate  of  the  vibra- 
tions set  up  in  the  part  percussed,  and  the  more  rapidly  these  vibra- 
tions occur,  the  higher  the  pitch,  and  vice  versa.  The  deep  rumble 
of  the  basso  and  the  high  "A"  of  the  soprano  exemplify  extremes  of 
low  and  of  high  pitch  respectively,  while  by  their  quality  the  sounds 
are  recognized  as  the  male  and  the  female  human  voices.  Other  con- 
ditions being  the  same,  a  tense  muscular  thorax  yields  a  percussion 
sound  of  higher  pitch  than  a  relaxed,  thin  chest,  and  the  same  is  true 


1 8  PHYSICAL   DIAGNOSIS 

of  a  small  thorax  in  comparison  with  a  large  one.  Similarly,  higher 
pitched  sounds  are  afforded  by  small  than  by  large  air-containing 
viscera,  cavities,  and  consolidations,  by  muscle  than  by  lung,  and 
by  pleural  effusion  than  by  pulmonary  infiltration. 

The  duration  of  a  sound,  which  is  an  element  of  subsidiary  impor- 
tance, expresses  simply  its  length  or  continuance.  Duration  and 
pitch  are  intimately  related,  in  that  the  lower  the  pitch,  the  longer 
the  duration,  and  vice  versa.  For  instance,  normal  low-pitched 
pulmonary  resonance  is  of  longer  duration  than  the  sound  obtained 
by  percussing  over  a  high-pitched  patch  of  pneumonic  or  tuberculous 
consolidation. 

Intensity,  or  volume,  also  of  secondary  importance,  refers  to  the 
degree  of  fulness,  loudness,  or  amplitude  of  a  sound.  It  goes  hand 
in  hand  with  the  foregoing  attributes,  pitch  and  duration,  especially 
with  the  latter — the  longer  the  duration  of  a  sound,  the  greater  its 
intensity.  Thus,  normal  pulmonary  resonance  yields  a  more  intense 
sound  than  a  consolidated  area,  while,  on  the  other  hand,  the  sound 
over  a  small  cavity  is  feebler  than  that  over  an  extensive  excavation. 
The  intensity  of  a  sound  is  determined  by  several  factors,  of  which 
the  most  important  are  the  force  of  the  percussion  stroke,  the  amount 
of  air  contained  in  the  part  percussed,  and  the  thickness  and  resiliency 
of  the  intervening  structures. 

Sense  of  Resistance. — The  resistance  appreciated  by  the  plexi- 
meter  finger  when  the  percussion  blow  is  delivered  is,  to  the  experi- 
enced clinician,  quite  as  certain  a  guide  as  the  actual  sound  elicited. 
This  resistance  is  a  particularly  useful  clue  in  ill-defined  pulmo- 
nary consolidations  in  which  exaggerated  fremitus,  frank  dulness, 
and  definite  auscultatory  signs  are  wanting,  and  in  such  instances 
a  high-pitched  sound  with  an  increased  feeling  of  resistance  is 
often  conclusive  evidence.  Percussion  of  the  thigh  gives  a  good 
example  of  greatly  increased  resistance,  and  over  the  colon,  an 
illustration  of  diminished  resistance.  The  resistance  is  strikingly 
exaggerated  over  a  pleural  effusion,  well  marked  over  a  consoli- 
dated lung,  and  usually  diminished  over  a  pneumothorax.  As  a 
general  rule,  it  may  be  stated  that  tactile  resistance  increases  part 
passu  with  the  extent  to  which  the  air  contained  in  an  organ  is  replaced 
by  liquid  or  solid  matter,  and  with  the  increase  in  the  tension  of  the 
parietal  structures. 

Tonal  Properties  of  the  Percussion-sound. — Resonance. — If  an 
air-containing  organ,  such  as  the  lung,  be  percussed,  the  sound  elicited 
has  a  clear,  soft,  resounding  quality,  a  moderately  low  pitch,  and  a 
well-sustained  duration  and  intensity.  This  typically  resonant  sound, 
or  pulmonary  resonance,  though  pure  and  clear,  lacks  the  harmony 


METHODS    AND    TECHNIC   OF    PHYSICAL   EXAMINATION      1 9 

and  consonance  of  a  true  musical  note,  for  it  is  caused  by  the  vibra- 
tions of  air-columns,  which,  owing  to  the  peculiarities  of  the  broncho- 
pulmonary  structures,  lack  precise  rhythm  and  equality  of  sound- 
waves. 

Tympany. — If  an  air-containing  organ,  such  as  the  stomach,  be 
percussed,  a  clear,  hollow  sound  is  produced,  differing  chiefly  from 
pulmonary  resonance  in  having  a  distinctive  drum-like  quality.  This 
tympanitic  resonance,  or  tympany,  is  a  typical  musical  note,  since  it 
is  due  to  rhythmic  vibrations  of  sound-waves  of  equal  length  occur- 
ring within  an  empty  cavity  bounded  by  thin,  smooth,  elastic  walls. 

Hyperresonance. — Percussion  of  an  overdistended  lung,  as  in 
hypertrophic  emphysema,  creates  a  sound  which,  though  it  retains  the 
quality  of  normal  pulmonary  resonance,  differs  from  it  in  possessing 
greater  intensity  and  lower  pitch.  Such  a  sound  approaches  tym- 
pany,  yet  it  cannot  be  so  designated,  because  it  lacks  the  true  tym- 
panitic or  drum-like  quality.  The  compromise  term,  hyperresonance, 
is,  therefore,  applied  to  this  tone,  used  to  signify  the  various  shades 
of  exaggerated  resonance  not  amounting  to  actual  tympany. 

Independent  of  the  above-mentioned  physical  causes  is  the  sound 
elicited  by  percussion  over  a  bony  structure,  which,  when  struck, 
vibrates  resonantly  by  virtue  of  its  inherent  resiliency,  and  emits  a 
sound  termed  osteal  resonance.  The  qualities  of  the  osteal  tone  are 
well  illustrated  by  percussion  over  the  sternum.  Auscultatory  per- 
cussion over  an  echinococcus  cyst  yields  a  peculiar  low-pitched  sonor- 
ous tone,  known  as  hydatid  resonance,  provided  that  the  cyst  is  super- 
ficial, and  contains  a  thin  liquid  inclosed  within  resilient  walls.  This 
sound  is  due  to  the  same  factors  responsible  for  hydatid  fremitus 
(q.  v.) ,  of  which  it  is  the  tonal  equivalent. 

Certain  forms  of  modified  resonance — amphoric,  cracked-pot,  and 
vesiculotympanitic — are  discussed  in  connection  with  the  special 
circumstances  under  which  they  occur.  (See  p.  146  et  seq.) 

Didness  and  Flatness. — These  two  words  express  varying  degrees 
of  impaired  resonance,  ranging  from  the  trifling  impurity  of  sound 
due  to  a  slight  diminution  of  air  in  a  part,  to  the  absolute  deadness 
found  over  an  entirely  airless  structure.  Flatness  is  the  acoustic 
acme  of  dulness,  and  between  the  two  extremes  numerous  tonal 
gradations  exist,  designated,  for  convenience  sake,  as  impaired  reso- 
nance and  relative  dulness. 

The  terms  dulness  and  flatness  are  not  to  be  used  synonymously: 
the  former  is  applied  to  a  sound  which,  though  impaired,  still  retains 
some  element  of  resonance,  and  the  latter  to  a  sound  to  which  even 
the  faintest  trace  of  resonance  is  foreign.  A  dull  sound  indicates 
that  the  air-content  of  the  part  within  range  of  percussion  is  dimin- 


20  PHYSICAL    DIAGNOSIS 

ished,  but  not  absolutely  abolished,  the  latter  condition  being  betrayed 
by  flatness.  For  example,  the  percussion-sound  over  a  patch  of 
pneumonic  hepatization  is  dull,  not  flat,  inasmuch  as  the  consolidated 
lung  is  not  entirely  deprived  of  air,  owing  to  the  fact  that  the  com- 
municating bronchi  and  many  groups  of  unimplicated  vesicles  con- 
tain a  sufficient  volume  of  air  to  emit  a  feeble  shade  of  resonance. 
On  the  other  hand,  a  pleural  effusion,  being  quite  airless,  affords  pure 
flatness  without  a  suspicion  of  resonance. 

According  to  their  acoustic  attributes,  it  will  be  noted  that,  as  the 
dull  percussion-sound  approaches  flatness,  the  quality  hardens,  the 
pitch  rises,  the  intensity  and  duration  diminish,  and  the  resistance 
increases.  A  slight  elevation  in  pitch  plus  increase  in  the  resistance 
over  the  part  percussed  is  one  of  the  earliest  signs  of  impaired  reso- 
nance, and,  since  it  is  usually  appreciable  before  the  development 
of  frank  dulness,  the  finding  is  most  pertinent. 

The  resonant  quality  of  an  air-containing  part  is  materially  modi- 
fied by  the  degree  of  tension  existing  in  its  walls,  which,  to  resound 
resonantly,  must  be  sufficiently  relaxed  to  vibrate  freely  under  the 
impact  of  the  percussion  blow.  Up  to  a  certain  point  of  mural  ten- 
sion the  sound  remains  clear,  but  if  the  tension  be  raised  beyond 
this  "resonant  point,"  the  purity  of  the  sound  disappears  and  it 
becomes  dulled  and  toneless.  In  a  similar  manner  undue  lowering 
of  the  mural  tension  dulls  a  resonant  sound. 

The  pitch  of  resonance  varies  according  to  the  volume  of  air  con- 
tained in  the  part  emitting  the  sound:  the  pitch  of  pulmonary  reso- 
nance, for  example,  rises  as  the  air-content  of  the  lung  is  lessened  by 
the  encroachment  of  a  consolidation,  as  in  croupous  pneumonia; 
the  pitch  of  the  note  is  higher  over  the  small  intestine  than  over  the 
large  gut. 

The  intensity  and  the  duration  of  resonance  are  determined  by 
the  force  and  the  length  of  the  sound-waves  within  the  part  per- 
cussed :  other  conditions  being  equal,  the  larger  the  air-space  within 
the  organ,  the  louder  and  the  more  lasting  the  sound  evoked  by  per- 
cussion. 

Aside  from  the  influences  of  mural  tension  and  air-volume  in  modify- 
ing the  resonance  of  an  air-containing  part,  the  force  of  the  percus- 
sion blow  and  the  vibratory  properties  of  the  tissues  within  its  range 
are  also  determining  factors  of  the  sound  produced. 

Spinal  Percussion. — Spinal  percussion  is  not  without  value  in 
the  study  of  obscure  lesions  of  the  lungs  and  mediastinum  lying 
close  enough  to  the  spine  to  damp  its  vibrations,  but  too  far  from  the 
thoracic  wall  to  produce  definite  dulness  thereupon.  Healthy  verte- 


METHODS    AND   TECHNIC    OF    PHYSICAL    EXAMINATION       21 

brae  emit  osteal  percussion-sounds  sui  generis  in  quality,  and  of  a 
degree  of  resonance  corresponding  to  the  extent  to  which  the  bone 
vibrations  are  affected  by  adjacent  anatomic  structures.  The  accom- 
panying diagram  (Fig.  4)  shows  a  clinical  modification  of  Koranyi's 
spinal  zones,  each  affording,  in  health,  distinctive  percussion  find- 
ings which  are  variously  altered  by  morbid  processes  of  the  thorax 
and  abdomen.  Thus,  the  normal  dulness  of  the  uppermost  zone 
diminishes  vertically  in  hypertrophic  emphysema,  but  lengthens  in 


^P^ 


V  I.-1V.  thoracic 
(dulness) 


>  V.-XII.  thoracic 
(osteal  resonance) 


Lumbar  (impaired 
resonance) 


Sacral  (flat  tympany) 


Fig.  4. — Spinal  percussion  zones. 

mediastinal  neoplasm  and  in  thoracic  aneurism.  Pulmonary  con- 
solidation may  appreciably  dull  the  osteal  resonance  of  the  thoracic 
zone,  while  fluid  within  the  pleural  sac  causes  dulness  at  the  base  of 
this  region  and  extending  thence  upward  to  a  height  commensurate 
with  the  volume  of  the  effusion.  (See  Grocco's  Triangle,  p.  273.) 
A  tumor  of  the  abdomen  (i.  e.,  hepatic,  splenic,  or  pancreatic)  may 
substitute  absolute  dulness  for  the  normal  impaired  resonance  of  the 
lumbar  zone  and  even  obliterate  the  flat  tympany  below.  Spinal  per- 
cussion is  usually  performed  with  the  aid  of  a  soft-rubber  plexor  and 


22  PHYSICAL    DIAGNOSIS 

vulcanite  pleximeter,  the  latter  being  placed  over  the  spinous  proc- 
esses, but  the  writer  prefers  to  use  ordinary  mediate  finger  percus- 
sion in  order  to  judge  tactile  resistance  as  well  as  tonal  changes. 

By  percussion  of  the  vertebral  tips  and  the  upper  interscapular 
region  Ewart  has  mapped  out  a  paravertebral  ovoid  subresonant 
area  between  the  first  and  the  fifth  thoracic  spines,  extending 
vertically  for  1 10  mm.  and  having  an  equatorial  diameter  of  90  mm., 
each  lateral  boundary  being  equidistant  from  the  midline.  This 
ovoid  patch  contracts  laterally  with  deep  inspiration  and  com- 
mensurately  expands  with  expiration.  In  apical  phthisis  and 
pleurisy  its  respiratory  excursions  are  restricted  and  its  sym- 
metry is  altered,  and  in  hypertrophic  emphysema,  in  addition, 
the  size  of  the  patch  is  greatly  diminished.  Extension  of  dul- 
ness  in  this  region,  with  modification  of  the  normal  ovoid  shape, 
has  been  reported  in  tracheobronchial  adenopathies,  in  peri- 
cardial  effusion,  in  extensive  enlargement  of  the  left  auricle,  in 
aortic  aneurysm,  and  in  enlarged  thymus. 

Vertebral  reflexes  (Abrams)  are  demonstrable  by  the  percussion 
of  appropriate  spinous  processes,  whereby  contraction  and  dilatation 
of  the  deep  viscera  are  provoked  if  the  organs  in  question  be  healthy. 
Upon  this  fact  depends  the  clinical  utility  of  the  test,  which  consists 
cf  outlining  the  organ,  by  topographic  percussion,  both  before  and 
after  vertebral  concussion,  and  of  comparing  the  size  of  the  two 
boundaries.  In  health,  percussion  of  the  lower  five  thoracic  spines 
should  enlarge,  and  of  the  vertebra  prominens  should  diminish,  the 
cardiac  and  aortic  areas  of  dulness  anteriorly,  while  percussion  of  the 
upper  three  lumbar  vertebrae  should  reflexly  contract  the  normal 
areas  of  the  liver,  the  spleen,  and  the  stomach.  Spinal  reflexes  are 
usually  evoked  by  delivering  a  few  sharp  blows  with  a  plexor  upon  the 
spinous  processes,  the  outline  of  the  organ  before  and  after  this 
manoeuver  being  judged  by  auscultatory  percussion. 

AUSCULTATION 

Auscultation,  as  applied  to  clinical  examinations,  is  the  act 
of  listening  to  physical  sounds,  normal  and  pathologic,  either  by 
the  aid  of  an  instrument  known  as  a  stethoscope,  or  by  applying 
the  ear  directly  to  the  part.  This  method  of  research  is  employed 
chiefly  in  investigating  the  condition  of  the  respiratory  system 
and  the  heart,  but  in  certain  instances  it  gives  useful  data  relat- 
ing to  the  arteries,  the  veins,  and  the  abdominal  organs.  Although 
Hippocrates,  who  observed  that  liquid  within  an  air-distended 
pleural  cavity  splashed  audibly  when  the  subject's  body  was  suddenly 


METHODS   AND    TECHNIC    OF   PHYSICAL   EXAMINATION      23 

shaken,  was,  in  a  strict  sense,  the  first  to  practise  auscultation,  this 
procedure  did  not  enjoy  clinical  vogue  until  the  time  of  Laen- 
nec's  publication,  in  1819,  of  his  Traite  de  V Auscultation  mediate.  In 
this  masterpiece  Laennec  described  his  new  invention,  the  stetho- 
scope, and  dealt  with  the  mechanism  of  auscultato'ry  signs  and  their 
application,  especially  to  diseases  of  the  heart  and  the  lungs,  his 
conclusions  upon  these  subjects  becoming  the  acknowledged  standard 
upon  which  subsequent  studies  were  based.  Of  the  many  investi- 
gators to  whom  our  present  knowledge  of  auscultation  is  due,  the 
names  of  Skoda,  of  Gerhardt,  of  Traube,  and  of  Wintrich  deserve 
noteworthy  prominence. 

Auscultation,  like  percussion,  may  be  either  mediate  or  immediate, 
according  to  whether  or  not  a  stethoscope  is  employed,  and  of  these 
two  methods,  the  former  is  chosen  in  the  great  majority  of  routine 
examinations.  In  the  exceptional  instance,  however,  the  naked  ear 
appreciates  certain  sounds  that  are  ill  denned,  if  not  quite  imper- 
ceptible, with  a  stethoscope,  so  that  to  be  equal  to  emergencies  of 
this  sort  one  must  train  one's  self  in  the  technic  of  both  methods  of 
auscultation.  As  Connor  has  pointed  out,  faint,  high-pitched  sounds 
are  indifferently  transmitted  by  closed  tubes,  particularly  by  tubes 
with  flexible  walls,  from  which  fact  it  follows  that  certain  cardiac 
murmurs  of  high  pitch,  blowing  quality,  and  feeble  intensity,  as  well 
as  vesicular  sounds  of  similar  characteristics,  are  heard  more 
clearly  by  auscultation  with  the  naked  ear  than  by  using  a  stetho- 
scope, particularly  one  of  the  binaural  pattern  with  two  flexible 
rubber  ear-tubes. 

Stethoscopic  auscultation  is  of  value  chiefly  in  the  investigation 
of  circumscribed  lesions  of  the  respiratory,  cardiovascular,  and 
abdominal  organs,  since  under  such  circumstances  it  is  important 
to  exclude  every  extraneous  noise  interfering  with  the  peculiarities 
of  the  sound  under  analysis.  Owing  to  their  contour,  certain 
areas  of  the  body  (i.  e.,  the  supraclavicular  and  infraclavicular  fossae 
and  the  upper  axillae)  can  be  examined  satisfactorily  only  with  a 
stethoscope,  while  this  instrument  also  comes  into  play  when  the 
patient's  modesty,  or  perchance  disregard  of  personal  hygiene,  forbids 
the  direct  application  of  the  ear  to  the  body,  even  if  some  covering  be 
interposed. 

The  Choice  of  a  Stethoscope. — In  the  practice  of  mediate  auscul- 
tation the  choice  of  that  form  of  stethoscope  best  suited  to  the  needs 
of  the  user  is  the  first  essential  of  success.  Naturally,  this  question 
must  be  decided  largely  upon  personal  grounds,  although  in  the 
selection  due  weight  should  be  given  to  certain  acknowledged  advan- 
tages peculiar  to  the  various  patterns  of  the  instrument. 


PHYSICAL   DIAGNOSIS 


Two  forms  of  stethoscopes  are  in  general  use — the  binaural  or 
double,  modified  to  a  greater  or  less  extent  from  the  design  originally 
suggested  by  Camman ;  and  the  monaural  or  single,  modeled  after 
the  original  instrument  invented  by  Laennec.  The  binaural  instru- 
ments designed  by  Bowles,  by  Sansom,  and  by  Arnold  are  well 
adapted  to  general  clinical  work,  while  Hawksley's  monaural  stetho- 
scope is  the  simplest  and  most 
convenient  pattern  of  this  type  of 
instrument. 

The  Bowles  stethoscope  consists 
of  a  steel,  cupped  chest-piece,  fitted 
with  a  hard-rubber  diaphragm,  and 
communicating,  by  means  of  flexi- 
ble rubber  tubing  and  a  Y-coupling, 
with  two  metal  conducting  tubes 
provided  with  ear-pieces  and  con- 
nected by  an  adjustable  steel  spring 
(Fig.  5) .  The  standard  disc-shaped 
chest-piece  is  made  in  two  sizes,  of 
which  the  smaller  is  preferable, 
owing  to  its  restriction  of  the  aus- 
cultatory  area  and  to  its  accurate 
adaptation  to  depressed  areas,  such 
as  the  intercostal  and  supraclavic- 
ular  spaces.  For  such  purposes  the 
small  disc  is  just  as  satisfactory  as 
the  special  "flat-iron"  chest-piece 
devised  for  this  sort  of  work. 
Bowles's  stethoscope  is  convertible 
into  an  ordinary  binaural  by  re- 
placing the  metal  chest-piece  by  a 
hard-rubber  bell,  also  furnished 
with  the  instrument. 

Personally,  the  author  prefers  to 
use  a  Bowles  stethoscope,  equipped 
Fig.  5-The  Bowles  stethoscope.         ^   ^^j^  ear-pieces,'    a    l±- 

inch  (3.75  cm.)  rubber-capped  disc,  and  i5-inch  (37.5  cm.)  lengths 
of  the  best  grade  of  flexible  catheter  tubing  (No.  14,  E).  The 
rubber  cap,  which  prevents  slipping  of  the  chest-piece  and  nega- 
tives metallic  tones,  can  be  cemented  to  the  disc  with  strong  fish- 
glue.  The  catheter  tubing,  of  the  dimensions  specified,  is  a  perfect 
1  Made  by  C.  H.  Liverpool  &  Co.,  Boston,  Mass. 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       25 

conductor  of  sounds,  and  so  flexible  that  it  cannot  kink.  It  is  suffi- 
ciently long  to  allow  adjustment  of  the  chest-piece  to  any  part  of 
the  back  of  a  patient  lying  in  dorsal  decubitus,  without  disturbing 
the  subject — a  distinct  advantage  when  examining  a  bed-ridden 
person  too  ill  to  be  turned  on  the  side.  Thus  equipped  (Fig.  5) ,  the 


Fig.  6. — Sansom's  binaural  stethoscope.  Fig.  7. — Arnold's  phonophore. 

instrument  can  be  depended  upon  to  amplify  sounds  without  undue 
exaggeration,  to  conduct  them  with  great  purity  and  clearness,  and 
to  facilitate  the  analysis  of  circumscribed  adventitious  sounds. 

Sansom's  stethoscope  (Fig.  6)  embodies  all  the  good  points  of  the 
older  types  of  binaural  stethoscope,  none  of  which,  it  may  be  added, 
is  so  satisfactory  for  routine  work  as  the  instrument  devised  by  Mr. 


26  PHYSICAL   DIAGNOSIS 

Bowles.  All  follow  the  same  general  principle — having  a  metal 
frame  adjusted  to  the  examiner's  head  by  the  pressure  of  a  spring, 
and  provided  with  ear-pieces  and  conducting  tubes  terminating  in 
a  chest-piece  made  of  hard  rubber,  of  wood,  or  of  metal.  In  most 
binaurals  the  metal  work  and  the  rubber  tubing  are  too  light,  the 
ear-pieces  ill  fitting,  the  chest-pieces  defective,  and  the  springs 
difficult  to  adjust  properly.  If  a  folding  stethoscope  (Fig.  6)  be 
preferred,  one  should  take  care  to  select  a  model  that  can  be  opened 
and  closed  without  straining  the  spring  and  frame,  and  that  is  pro- 
vided with  a  spring  joint  of  stout  construction  and  of  firm  locking 
action  which  does  not  rattle  when  the  instrument  is  in  use. 

Arnold's  phonophore  (Fig.  7),  made  in  both  binaural  and  mon- 
aural models,  is  especially  helpful  in  listening  to  faint  high-pitched 
sounds,  which,  as  a  rule,  it  transmits  very  clearly ;  to  other  sounds,  how- 
ever, this  instrument  seems  to  lend  a  hollow,  somewhat  metallic 
quality,  and,  to  one  unaccustomed  to  its  use,  an  unnatural  intensity. 
The  phonophore  is  excellently  made,  having  soft-rubber  ear-pieces, 
heavy  metal  and  rubber  tubing,  and  a  resonating  steel  chest-piece 
the  sharp  edge  of  which  is  fitted  with  a  rubber  cushion. 

The  differential  stethoscope  is  a  form  of  instrument  equipped  with 
two  separate  chest-pieces  communicating,  by  individual  conducting 
tubes,  one  with  the  right  and  the  other  with  the  left  ear  of  the  auscul- 
tator.  It  is  of  service,  say  those  who  use  it,  in  timing  and  in  detecting 
quality  differences  of  cardiac  murmurs  produced  synchronously  at 
different  valve  areas,  by  applying  one  chest-piece  to  one  area  and 
the  other  to  another  locality,  and  discrimi- 
nating between  the  differences  in  the  tone 
and  rhythm  of  each. 

Ha-wksley's  monaural  stethoscope  (Fig.  8) 
consists  of  a  hard-rubber  ear-plate  screwed 
into  a  rigid  metal  tube  flaring  at  its  other 
extremity  into  a  bell-shaped  chest-piece,  or 
fitted  with  a  detachable  bell  made  of  vul- 
canite or  of  ebony.  This  pattern  of  stetho- 
A  scope  is  preferred  by  some  clinicians, 

notably  by  those  of  the  older  school,  who 
Flg'  aurld^eThio^e.111011"  claim  that  il  transmits  sounds  with  more 
distinctness,  greater  purity,  and  less  arti- 
ficial intensity  than  instruments  of  the  binaural  model.  The 
single  stethoscope,  though  excellent  in  some  respects,  is  inconvenient 
and  fatiguing  to  use  while  examining  a  patient  confined  to  bed, 
and  is  unsuited  for  auscultating  the  upper  thorax  and  the  lower 


T 


METHODS    AND    TECHNIC    OF   PHYSICAL    EXAMINATION      27 

abdomen.  It  is  not  clear  that  the  single  stethoscope  serves  any 
purpose  not  better  served  by  an  instrument  provided  with  flexible 
tubing  and  two  ear-pieces. 

Technic. — The  posture  of  the  patient,  dictated  by  the  nature  of 
the  examination,  should  be  as  unconstrained,  relaxed,  and  easy  as 
possible.  This  is  no  minor  essential,  especially  in  a  self-conscious, 
nervous,  or  feeble  person,  to  whom  even  the  simple  procedure  of 
auscultation  may  be  an  ordeal  sufficient  to  excite  unnatural  breathing, 
artificial  muscular  rigidity,  and  curious  cardiac  irregularity,  all  of 
which  defects  are  exaggerated  by  a  constrained,  uncomfortable  posi- 
tion. As  in  percussing,  auscultating  should  not  be  needlessly  pro- 
longed. 

In  mediate  auscultation  the  stethoscope  should  be  applied  to  the 
naked  surface  of  the  body,  for,  unless  preternaturally  gifted,  the 
average  physician  is  unable  to  detect  delicate  acoustic  differences 
through  the  patient's  clothing,  the  rustling  and  creaking  and  dulling 
effect  of  which  may  effectually  modify,  if  not  entirely  mask,  important 
auscultatory  findings. 

The  chest-piece  of  a  binaural  instrument  should  be  applied 
lightly  and  evenly  to  the  surface  over  the  area  under  examina- 
tion, being  approximated  thereto  by  the  pressure  of  one  or  two 
fingers,  which  must  not  bear  too  heavily,  lest  the  undue  pressure 
thus  exerted  extinguish  certain  ill-defined  sounds  audible  only  when 
the  stethoscope  rests  lightly  upon  the  surface.  As  Sewall  points 
out,  stethoscopic  pressure  with  the  chest-piece  of  an  instrument 
designed  to  transmit  purely  by  air  conduction  has  a  distinct  effect 
upon  the  character  of  the  auscultated  sounds,  which  are  made 
up  of  two  separate  components — visceral  tones  and  mural  vibra- 
tions. Of  the  two,  the  latter  generally  predominate,  and  are  more 
or  less  effectually  effaced  by  firm  pressure.  In  general,  stethoscopic 
pressure,  when  it  does  not  quite  annul  the  voice  sounds  and  the 
respiratory  murmur,  dulls  them,  raises  their  pitch,  and  lends  to 
them  a  tinge  of  the  bronchial  tone,  modifications  due  perhaps  to 
pressure-dampening  of  the  fundamental  lower  vibrations  of  the 
parietes.  This  modification  is  particularly  true  when  pressure  is 
made  over  the  lower  part  of  the  thoracic  wall.  Emerson  has  shown 
that  sounds  produced  at  the  parietes  (i.  e.,  faint  tones  of  the  heart; 
indistinct  murmurs  of  mitral  obstruction;  the  fetal  heart-beats) 
are  easily  damped  by  the  pressure  of  the  stethoscope,  while  cer- 
tain transmitted  sounds  (i.  e.,  high-pitched  rales;  blowing  cardiac 
murmurs)  are  made  clearer  thereby.  With  a  monaural  stethoscope, 
held  in  position  by  the  pressure  of  the  examiner's  head,  it  is  espe- 


28  PHYSICAL   DIAGNOSIS 

cially  difficult  to  observe  these  niceties  of  adjustment,  and,  moreover, 
when  firm  pressure  is  necessary,  the  chest-piece  is  likely  to  indent 
the  subject's  chest  and  cause  considerable  discomfort.  Whichever 
model  is  used,  the  chest-piece  must  be  held  snugly  in  contact  with 
the  skin,  so  that  the  auscultator  will  not  be  confused  by  hearing 
extrinsic  noises,  amazingly  magnified,  which  otherwise  leak  in;  in 
emaciated  subjects  and  in  those  with  very  narrow  interspaces  it  is 
sometimes  necessary  to  use  a  soft-rubber  chest-piece  to  insure  an 
air-tight  contact. 

Only  the  tyro  need  be  warned  against  confusing  with  adventitious 
sounds  certain  rude,  jarring  noises  due  to  slips  in  technic,  such  as 
movements  of  the  examiner's  fingers  over  the  metal  parts  of  the 
stethoscope,  accidental  contact  of  the  rubber  tubing  with  nearby 
objects,  and  friction  between  the  chest-piece  and  a  dry,  hairy  skin. 
In  addition  to  these  extrinsic  sounds,  one  must  recognize  various 
noises  produced  by  contraction  and  respiratory  movements  of  the 
surface  muscles,  particularly  of  the  upper  anterior  thorax. 

Transmanual  auscultation,  suggested  by  Riesman  to  facilitate  the 
timing  of  cardiac  murmurs,  consists  of  auscultating  through  the 
hand  laid  over  the  precordia,  whereby,  if  the  apex-beat  be  palpable, 
it  is  possible  to  feel  the  systolic  impact  of  the  heart  and  to  hear  an 
endocardial  murmur  at  the  same  time  and  place.  With  a  Bowles 
stethoscope  there  is  no  difficulty  in  distinguishing  cardiac  sounds 
through  the  intervening  hand,  and  this  combined  method  of  pal- 
pation and  auscultation  is  of  distinct  value,  especially  in  differen- 
tiating presystolic  and  systolic  bruits  generated  at  the  mitral  orifice 
of  the  heart. 

Acromion  auscultation  (Abrahams),  with  the  bell  of  the  stetho- 
scope applied  to  the  outer  end  of  the  clavicle,  is  useful  in  studying 
obscure  apical  sounds  which  are  amplified  and  well  transmitted 
by  the  conducting  properties  of  the  underlying  bone. 

The  technic  of  immediate  auscultation  is  obviously  too  simple  to 
call  for  detailed  description,  though  it  is  not,  perhaps,  out  of  place 
to  suggest  that  the  auscultator  should  invariably  cover  the  region 
under  examination  with  a  thin  towel  or  other  suitable  material 
before  applying  the  ear  to  the  part. 

Phonometry. — The  method  of  phonometry,  by  means  of  which 
the  examiner  aims  to  ascertain  the  condition  of  different  organs  by 
the  tone  of  a  tuning-fork  placed  on  the  surface,  deserves  recognition 
as  a  useful  clinical  aid.  As  elaborated  by  Habershon,  by  Benedict, 
and  more  recently  by  Cantlie,  the  examiner  auscultates  with  a  bin- 
aural  stethoscope  over  a  solid  or  a  hollow  organ  to  the  vibrations 


METHODS    AND   TECHNIC    OF   PHYSICAL   EXAMINATION      29 

of  a  tuning-fork  applied  to  the  surface  of  the  body  over  such  an 
organ,  and  systematically  moved  so  as  to  cross  its  outer  bounda- 
ries. When  this  occurs,  the  sound  originally  heard  suddenly  grows 
faint  or  is  quite  inaudible,  as  the  vibrations  pass  from  the  auscul- 
tated area  to  neighboring  parts,  and  the  observer  is  thus  enabled 
to  delimit  the  part  by  pencilling  upon  the  skin  the  points  at  which, 
this  change  of  sound  occurs.  A  fork  with  a  narrow  blunt  handle 
and  with  long  vibrating  prongs  tuned  to  a  note  of  G  sharp  serves 
best  for  general  purposes.  Tuning-fork  auscultation  is  applied 
to  the  outlining  of  pleural  effusions  of  fluid,  and  to  delimiting  solid 
organs  such  as  the  liver,  the  heart  and  the  spleen,  and  air-filled 
viscera  like  the  stomach  and  the  large  intestine. 

The  term  autophonometry  is  applicable  to  a  procedure  based 
upon  vibrating  sensations  appreciated  by  the  subject  when  the 
handle  of  a  vibrating  tuning-fork  is  applied  to  the  surface  of  the 
body,  this  method  having  been  used  to  demonstrate  pulmonary 
consolidations,  as  well  as  in  the  study  of  certain  lesions  attended  by 
diminished  cutaneous  sensibility.  Stritch  has  shown  that  the  patient 
feels  these  vibrations  most  distinctly  when  the  instrument  is  placed 
over  a  dull  area  of  the  thorax,  less  distinctly  when  over  an  impaired 
area,  and  least  over  normal  pulmonary  resonance.  When  a  tuning- 
fork  is  placed  upon  various  subcutaneous  bony  prominences  (i.  e., 
the  sternum,  malleoli,  styloid  process  of  the  ulna,  and  nails  of  the 
fingers  and  toes)  the  vibrating  sense  is  commonly  abolished,  often 
before  cutaneous  sensibility  is  impaired,  in  patients  affected  with 
peripheral  neuritis,  locomotor  ataxia,  spinal  caries,  syphilis  of  the 
cord,  and  diabetes  mellitus. 


THORACOMETRY  AND  CYRTOMETRY 

The  tape-measure  and  calipers,  which  should  be  graduated  in 
inches  and  in  centimeters,  are  employed  for  measuring  various  cir- 
cumferences and  diameters,  especially  of  the  thorax  and  abdomen, 
for  ascertaining  the  size  of  surface  lesions,  and  for  defining  the  exact 
position  of  local  physical  signs  with  reference  to  fixed  anatomic 
landmarks. 

Thoracometry,  or  mensuration  of  the  thorax,  has  for  its  chief 
objects  the  determination  of  the  girth  and  the  several  diameters  of 
the  chest.  In  taking  the  girth,  the  tape  should  incircle  the  chest 
horizontally  at  the  level  of  the  nipples,  and  the  measurements  noted 
during  respiratory  repose,  extreme  inspiration,  and  extreme  ex- 
piration, the  difference  between  the  last  two  expressing  the 


3°  PHYSICAL   DIAGNOSIS 

chest  expansion,  which  ordinarily  amounts  to  from  two  to  five 
inches  (5  to  12.5  CITI.)  in  a  healthy  man.  Various  stethometers, 
indicating  the  thoracic  excursions  upon  a  graduated  dial,  are 
available  for  measuring  the  chest  expansion,  but  the  simple 
tape-line  is  quite  as  accurate  as  any  of  these  instruments.  Com- 
parative measurements  of  the  two  halves  of  the  chest  are  made  by 
half-circling  each  side  from  midsternum  to  midspine,  care  being 
taken  to  follow  precisely  the  same  horizontal  level  and  to  apply  the 
tape  with  equal  tension  on  both  sides.  In  comparing  the  semi- 
circumferences  thus  obtained,  allowance  must  be  made,  in  right- 
handed  persons,  for  at  least  a  one-half  inch  (1.25  cm.)  greater 
measurement  on  the  right  than  on  the  left  side.  In  measuring 
abdominal  girths  the  tape  is  generally  passed  horizontally  around 
the  belly  at  the  level  of  the  umbilicus. 

It  is  convenient  to  take  as  the  vertical  diameter  of  the  chest  the  dis- 
tance from  the  highest  point  of  the  axilla  to  the  lowest  level  of  the 
costal  margin,  and  to  measure  the  two  horizontal  diameters  at  the 
level  of  the  nipples;  the  anteroposterior  diameter  is  found  by  applying 
one  point  of  the  caliper  to  the  median  line  of  the  sternum  and  the 
other  point  to  a  vertebral  spine,  and  the  transverse  diameter  by  caliper- 
ing  the  chest  between  two  corresponding  points  upon  the  lateral 
walls  in  the  midaxillae. 

Cyrtometry,  or  the  procedure  of  outlining  body-curves,  is  applic- 
able chiefly  to  determining  the  shape  of  the  thorax  in  cross-section. 
For  this  purpose  numerous  more  or  less  elaborate  cyrtometers  have 
been  devised,  none  of  which  is  more  satisfactory  than  a  simple 
instrument  made  of  two  narrow,  flat  strips  of  soft  lead,  each  two  feet 
(60  cm.)  in  length,  and  hinged  together  with  a  bit  of  rubber  tubing. 
Having  adjusted  this  hinge  to  the  spine,  the  chest  is  incircled  hori- 
zontally by  the  strips,  which,  being  flexible,  can  be  molded  accurately 
to  the  body;  having  thus  taken  an  impression  of  the  entire  circum- 
ference of  the  chest,  the  strips  are  removed  by  slipping  them  from  their 
rubber  connection,  each  section  retaining  the  contour  of  the  surface 
to  which  it  was  molded.  A  pencil  tracing  of  the  strips  after  their 
removal  gives  a  graphic  transverse  section  of  the  chest,  and  may  be 
the  means  of  revealing  deviations  from  the  normal  contour  too  trivial 
to  attract  attention  on  casual  inspection.  Cyrtometry  is  useful  both 
as  a  means  of  initial  diagnosis  and  in  studying,  from  permanent 
records,  the  progress  of  thoracic  development  and  retrogression  in 
persons  affected  with  chronic  pulmonary  lesions. 


METHODS    AND    TECHNIC    OF   PHYSICAL   EXAMINATION      31 

SPHYGMOMANOMETRY 

Sphygmomanometry,  or  the  instrumental  estimation  of  the 
arterial  blood-pressure,  shows  the  degree  of  arterial  tension  with 
far  greater  accuracy  than  simple  feeling  of  the  pulse  affords,  and 
serves  also  to  confirm  the  details  of  the  sphygmographic  tracings. 
The  sphygmomanometer,  used  for  gaging  the  tension,  is  based 
upon  the  principle  of  measuring  with  a  manometer  the  degree  of 
pressure  required  to  obliterate  the  pulse  of  a  part  distal  to  a  given 
point  of  constriction,  the  result  being  expressed  in  millimeters  of 
mercury.  A  pneumatic  constricting  armlet,  an  inflating  apparatus, 
and  a  mercurial  manometer  comprise  the  essential  working  parts 
of  the  instrument,  of  which  the  model  designed  by  Nicholson  is 
wrell  suited  for  clinical  work,  inasmuch  as  it  registers  both  systolic 
and  diastolic  pressures,  and  is  accurate,  simple,  and  portable. 
Rogers'  aneroid  sphygmomanometer,  which  registers  the  pressure 
by  an  aneroid  gage,  is  much  simpler  than  any  of  the  mercurial 
manometers,  and  is  sufficiently  accurate  for  routine  clinical  work. 
Hill  and  Barnard's  sphygmometer  is  useful  for  determining 
roughly  the  systolic  pressure,  in  much  the  same  way  that  one  some- 
times estimates  a  hemoglobin  percentage  with  a  Tallquist  scale, 
instead  of  with  a  more  elaborate  hemoglobinometer.1 

Technic  of  Sphygmomanometry. — The  working  parts  of  Nich- 
olson's sphygmomanometer  are  housed  in  a  metal  case,  the  lid  of 
which,  when  raised,  locks  automatically  and  firmly  supports  the 
whole  device  (Fig.  9).  When  shut,  the  instrument  fits  into  a 
leather  case,  with  the  armlet  and  inflating  bulb,  and  can  be  con- 
veniently carried  in  a  coat  pocket.  The  apparatus  consists  of  a 
steel  mercury  reservoir,  fitted  above  with  a  metal  Y-connection  for 
the  inflation  device  and  terminating  below  in  a  glass  mercury 
tube,  alongside  of  which  is  mounted  an  adjustable  scale  showing 
millimeter  divisions.  A  soft  pneumatic  armlet,  for  application  to 
the  patient's  arm,  is  connected  by  rubber  tubing  to  one  end  of  the 
Y-connection,  to  the  other  end  of  which  fits  a  tube  leading  from 
the  inflation  bulb,  which  carries  a  stop-cock  and  a  delicate  needle- 
valve  for  controlling  the  pressure  within  the  armlet.  Before  ad- 
justing the  latter  it  is  customary  in  hospital  work  to  place  the 

1  Nicholson's  sphygmomanometer  (Precision  Thermometer  and  Instrument 
Co.,  Philadelphia)  costs  $15.00;  Rogers'  (Taylor  Instrument  Companies, 
Rochester),  $25.00;  and  Hill  and  Barnard's  sphygmometer  (J.  J.  Hicks,  London) 
sells  for  $3.10  plus  duty.  The  original  Riva-Rocci  sphygmomanometer,  and 
the  modifications  thereof  suggested  by  Erlanger,  Mummery,  Martin,  and  others 
can  be  furnished  by  Hawksley  and  Son,  London. 


32  PHYSICAL   DIAGNOSIS 

subject  in  dorsal  recumbency,  with  the  arm,  relaxed  and  bared  to 
the  shoulder,  supported  by  a  pillow  at  the  level  of  the  heart.  The 
inflation  device  having  been  applied  to  the  arm,  with  the  rubber 
bag  over  the  brachial  artery,  the  remainder  of  the  armlet  is  wound 
smoothly  around  the  arm  and  the  end  tucked  under  the  last  turn, 
so  as  to  hold  it  in  place  when  pressure  is  established.  The  con- 


Fig.  9. — Nicholson's  sphygmomanometer.    The  auscultatory  method  of  estimating 

blood-pressure. 

nection  between  the  inflation  device  and  the  mercury  chamber 
having  been  made,  the  zero  mark  of  the  scale  is  adjusted  to  the 
level  of  the  top  of  the  mercury  column  in  the  glass  tube,  and 
inflation  is  begun,  with  the  stop-cock  parallel  to  the  tube  and 
the  needle- valve  closed.  Air  is  thus  forced  into  the  armlet  until 
the  radial  pulse,  meanwhile  being  palpated  with  the  examiner's  dis- 
engaged hand,  is  extinguished.  When  the  pulse  at  the  wrist  is  no 


METHODS    AND    TECHNIC    OF   PHYSICAL   EXAMINATION      33 

longer  appreciable,  the  release  valve  is  cautiously  opened  until 
the  mercury  column  (now  high  in  the  tube)  begins  to  fall.  The  level 
reached  by  the  mercury  column  at  the  moment  the  pulse  reappears 
indicates  the  systolic  pressure,  which  in  the  healthy  adult  usually 
ranges  between  120  and  140  mm.,  rarely  exceeding  the  latter  figure 
in  a  young  man,  and  being  from  25  to  50  points  lower  in  children 
under  two  years  old.  As  the  mercury  falls  its  oscillations  progres- 
sively increase  to  an  acme  and  then  diminish,  the  base  line  of  the 
maximum  oscillation  being  taken  as  the  degree  of  diastolic  pressure, 
which  varies  normally  from  about  90  to  no  mm.  in  adults,  or  ap- 
proximately 30  points  lower  than  the  systolic  pressure.  This  read- 
ing should  not  be  made  until  the  mercury  column  has  had  time 
to  adjust  itself  after  each  fall,  several  fluctuations  being  observed 
at  the  various  levels.  The  difference  between  the  systolic  and  the 
diastolic  figures  represents  the  pulse  pressure,  a  value  normally  ap- 
proximating from  20  to  30  mm. 

The  auscultatory  method  (Korotkow)  has  of  recent  years  largely 
replaced  the  original  palpatory  or  oscillatory  technic,  just  de- 
scribed. It  is  carried  out  by  stethoscopic  auscultation  of  the 
artery  at  a  point  below  the  cuff,  while  gradually  releasing  the  press- 
ure upon  the  vessel,  the  primary  object  being  the  detection  of  the 
following  series  of  sounds  as  the  compressed  artery  refills  with 
blood,  with  the  escape  of  air  from  the  armlet:  (i)  A  loud  clear  tone, 
coincident  with  the  first  inflow  of  blood  into  the  relaxed  vessel; 
(2)  multiple  murmurs  generated  by  local  blood  eddies;  (3)  a  second- 
ary sharp  sound,  changing  gradually  to  (4)  an  indistinct  dull  tone, 
caused  by  mural  vibrations  and  followed  by  (5)  complete  silence, 
as  the  normal  relations  of  blood  volume  to  vessel  lumen  are  re- 
stored. The  height  of  mercury  column  when  the  first  clear  tone 
is  heard  is  taken  as  the  systolic  pressure,  which  by  this  method  is 
some  10  or  15  points  higher  than  by  the  palpatory;  and  the  figure 
registered  at  the  time  of  the  dull,  muffled  tone  is  generally  conceded 
to  indicate  the  diastolic  pressure.  The  special  stethoscope  and 
tambour1  devised  by  Oliver  is  most  useful  in  determining  blood- 
pressures  by  the  auscultatory  method. 

Rogers1  sphygmomanometer  (Fig.  10)  consists  of  an  aneroid  man- 
ometer registering  on  a  dial  reading  from  o  to  300  millimeters  Hg, 
and  of  an  armlet  containing  a  rubber  pressure-bag  and  connecting, 
by  two  rubber  tubes,  with  the  gage  and  with  an  inflating  bulb. 
The  tube  leading  from  the  latter  is  provided  with  a  release  valve, 

1  Price,  $6.25,  duty  paid  (Hawksley  &  Son,  London). 


34  PHYSICAL   DIAGNOSIS 

for  relieving  the  armlet  compression.  The  armlet,  to  be  applied 
like  a  roller  bandage,  is  held  in  place  by  tucking  the  small  free 
end  under  the  preceding  fold,  the  pressure  produced  by  the  in- 
flating bulb  being  sufficient  to  keep  it  snugly  adjusted  to  the 
subject's  arm  during  the  observation.  The  aneroid  gage  is  then 
suspended  from  a  hook  on  the  outer  face  of  the  armlet,  and  the 
two  rubber  tubes  are  connected,  one  with  the  gage  and  the  other 
with  the  inflation  bulb.  To  obtain  the  systolic  pressure,  the  armlet 


Fig.  10. — Rogers'  sphygmomanometer.     The  palpatory  method  of  estimating  blood- 
pressure. 

is  inflated  by  means  of  the  bulb  until  the  compression  thus  produced 
obliterates  the  radial  pulse,  after  which  i  or  2  c.c.  additional  pres- 
sure is  added.  Now,  by  careful  manipulation  of  the  release  valve, 
air  is  permitted  to  escape  until  the  radial  beats  reappear,  the 
figure  registered  on  the  dial  at  this  exact  moment  representing  the 
systolic  pressure.  To  gage  the  diastolic  pressure  the  air  is  released 
very  slowly  until  the  dial  indicates  a  maximum  range  of  oscilla-, 
tions,  whereupon  the  valve  is  quickly  closed,  and  the  minimum  oscil- 
lation figure  taken  as  the  diastolic  value.  Rogers'  sphygmomanom- 
eter reads  within  about  5  mm.  of  the  figures  of  the  mercurial 
instruments,  over  which  it  possesses  the  advantages  of  greater 
simplicity,  ease  of  operation,  and  adjustability  for  differing  barom- 
etric conditions. 

Hill  and  Barnard's  sphygmometer  consists  of  a  glass  gage  gradua- 
ated  in  millimeters,  and  fitted,  by  a  short  length  of  rubber  tubing,  to 
a  small  rubber  ball  contained  in  a  silk  bag  (Fig.  1 1) .  The  gage  is 
closed  at  one  end  by  a  metal  cap  pierced  by  a  small  orifice,  which, 
by  manipulating  a  screw,  can  be  opened  and  closed.  By  means  of  this 
device  a  fluid  meniscus  can  be  produced  within  the  lumen  of  the 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       35 

tube  by  placing  its  open  end  in  water  (or  in  ink)  and  screwing  the 
column  up  and  down  until  the  top  of  the  fluid  reaches  the  zero  mark. 
This  accomplished,  the  rubber  ball  is  distended  with  air,  connected 
with  the  gage,  and,  covered  with  the  palm  of  one  hand,  pressed  down 


Fig.    ii. — The  Hill-Barnard  sphygmometer. 

firmly  upon  the  subject's  radial  artery,  the  beats  of  this  vessel  being 
meanwhile  felt  with  a  finger  of  the  examiner's  other  hand  at  a  point 
peripheral  to  the  rubber  ball.  The  figure  indicated  by  the  fluid 
when  the  radial  pulse  is  obliterated  is  taken  as  the  systolic  pressure. 
Hill  and  Barnard's  instrument  is  not,  of  course,  intended  to  do  the 
work  of  the  more  accurate  armlet-and-bulb  sphygmomanometer,  but 
its  simplicity  and  extreme  compactness  recommend  its  employment 
when  only  a  general  idea  of  the  blood-pressure  value  is  desired,  and 
under  circumstances  when  a  more  elaborate  method  of  sphygmo- 
manometry  is  impracticable. 

To  insure  accuracy,  the  blood-pressure  should  be  investigated 
only  when  the  subject  is  absolutely  at  rest,  both  physically  and 
mentally,  for  no  reading  shows  a  true  value  unless  obtained  when 
the  influence  of  transient  circulatory  stimuli  can  be  excluded — mus- 
cular tension,  intellectual  effort,  excitement,  fear,  all  raise  arterial 
pressure.  Smoking  a  strong  cigar  may  do  the  same,  but  alcohol 


36  PHYSICAL   DIAGNOSIS 

has  no  material  effect,  save  when  taken  too  liberally,  in  which  event 
the  pressure  falls  perceptibly.  Comparative  estimates  should  be 
made  under  precisely  similar  conditions,  relating  especially  to  the 
subject's  posture,  to  the  time  of  day,  and  to  the  technic  of  the 
armlet  application  and  other  details. 

The  practical  application  of  sphygmomanometry  and  the  patho- 
logic variations  of  arterial  blood-pressure  are  considered  subse- 
quently. It  is  sufficient  here  to  associate  hypertension  with  arterio- 
sclerosis, cardiac  hypertrophy,  renal  sclerosis,  and  the  toxic  states 
attending  gout,  plumbism,  syphilis,  and  other  specific  infections. 
Prominent  factors  of  hypotension  include  shock,  hemorrhage,  vom- 
iting, diarrhea,  anemia,  enteric  fever,  tuberculosis,  and  various 
lesions  of  the  heart  marked  by  myocardial  enfeeblement  and 
dilatation. 

The  term  "energy  index"  (Barach)  is  used  to  indicate  the  total 
efforts  per  minute  exerted  by  the  cardiovascular  system.  This 
figure,  which  in  health  approximates  20,000  mm.  of  mercury,  b 
calculated  by  multiplying  the  sum  of  the  systolic  and  the  diastolic 
pressures  by  the  pulse-rate.  Tigerstedt  judges  the  actual  pumping 
efficiency  of  the  heart  by  dividing  the  pulse-pressure  by  the  sys- 
tolic pressure;  the  figure  normally  reads  from  25  to  35  per  cent. 

Hoffmann,  in  1906,  suggested  the  use  of  the  sphygmomanometer 
in  the  study  of  the  pulsus  alternans  (q.  v.) ,  in  which  type  of  arhy th- 
mia  a  systolic  manometer  pressure  may  be  reached  which  obliter- 
ates the  alternately  feeble  impulses,  and 'thus  halves  the  pulse- 
rate  at  the  wrist.  In  such  instances  the  auscultatory  method  of 
tonometry  affords  at  high  pressures  but  one-half  of  the  tones  aud- 
ible when  the  armlet  is  deflated. 

By  Oliver's  method  the  venous  pressure  can  be  estimated  merely 
by  noting  at  what  height  above  the  level  of  the  cardiac  apex  the 
veins  on  the  dorsum  of  the  hand  collapse,  when  the  hand,  with 
fingers  extended,  is  held  vertically  and  slowly  raised.  If  the  sub- 
ject has  prominent  veins,  it  is  easy  to  distinguish  their  sudden 
collapse,  which  occurs  normally  at  a  height  of  f  inch  above  the 
apical  level.  The  height,  in  inches,  at  which  this  occurs  above  the 
apex  is  multiplied  by  2,1  to  indicate — and  with  surprising  accuracy 
— the  venous  pressure  in  millimeters  of  mercury. 

Although  no  direct  proof  of  a  venomotor  nervous  system  is 
available,  recent  physiologic  work  suggests  the  hypothesis  that  a 
mechanism  of  this  sort  exists,  comparable  to  the  general  vasomotor 

1  One  inch,  or  25.5  mm.,  represents  about  2  mm.  Hg  (1.985),  reckoning  the 
specific  gravity  of  the  blood  and  of  mercury  as  1.060  and  13.57,  respectively. 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       37 

system  (Yandell  Henderson).  The  studies  of  Hooker  show  that 
the  normal  venous  pressure  and  the  alterations  in  arterial  pressure 
are  independent.  With  laboratory  instruments  Howell  approxi- 
mates the  normal  venous  pressure  of  the  adult  at  about  7.5  cm.  of 
water;  while  Hooker's  figures  read  10  to  20  cm.  during  the  day  and 
7  to  8  cm.  during  sleep  at  night.  High  readings  are  common  in 
arteriosclerosis  and  in  the  failing  compensation  of  various  cardiac 
diseases;  well-compensated  lesions,  whether  muscular  or  valvular, 
produce  no  deviation  from  the  normal  figure. 

SPHYGMOGRAPHY.AND  CARDIOGRAPHY 

Graphic  records  of  arterial  and  venous  pulse-waves,  of  the  cardiac 
apex-beat,  and  of  other  pulsations  upon  the  surface  of  the  body  are 
obtainable  by  the  use  of  special- instruments  devised  for  the  purpose 
of  registering  surface  undulations.  For  recording  these  different 
pulsations  synchronously,  some  form  of  polygraph  is  necessary, 
such  an  instrument  consisting  essentially  of  a  series  of  delicate  levers, 
each  tipped  with  a  stilet  and  attached  to  a  separate  tambour,  com- 
municating by  rubber  tubing  with  a  cup-shaped  capsule  or  receiver, 
which,  when  placed  over  a  pulsating  area,  transmits  the  undulations 
thereof  to  its  respective  stilet.  The  latter  rests  upon  the  surface  of 
a  strip  of  smoked  paper,  driven  by  clockwork  at  uniform  speed  past 
the  stilet  point,  whose  oscillations  are  thus  scratched  upon  the  car- 
bonized film  as  a  graphic  tracing.  A  chronograph,  or  time-marker, 
is  also  useful  in  accurately  indicating  the  time-incidence  of  the  several 
tracings.  The  polygram  made  in  this  manner  is  suitably  labeled 
by  writing  upon  its  smoked  surface  with  a  dry  point,  after  which 
is  flooded  with  tincture  of  benzoin  or  with  negative  varnish,  hung 
up  until  dry,  and  subsequently  filed  with  the  case-history. 

Technic  of  Sphygmocardiography. — Of  the  several  polygraphs 
now  in  vogue,  Jaquet's  model  is  to  be  preferred  for  clinical  work  if 
its  high  cost  is  not  prohibitive,1  since  this  instrument  is  compact, 
comparatively  easy  to  operate,  and  capable  of  registering  three 
synchronous  tracings,  which,  though  they  may  seem  miniatures  of 
those  made  by  a  large  laboratory  kymograph,  show  all  essential 
details.  Marey's  polygraph,2  practically  unused  in  this  country, 
is  an  accurate,  though  somewhat  bulky,  instrument,  of  more  moderate 
price.  Gibson's  clinical  polygraph,3  which  takes  four  simultaneous 

1  Price,  $130.00,  duty  paid  (Arthur  H.  Thomas  Co.,  Philadelphia). 

2  Price,  $120.00,  duty  paid  (Charles  Verdin,  Paris). 

3  Price,  $146.40,  duty  paid  (T.  Hawksley,  London). 


38  PHYSICAL   DIAGNOSIS 

ink-tracings  on  glazed  paper,  is  even  more  expensive  than  either  of 
the  two  just  mentioned.  Dudgeon's  sphygmograph,1  adapted  to 
recording  but  a  single  tracing,  is  used  for  making  sphygmograms  of 
the  radial  pulse.  Equipped  with  Mackenzie's  polygraph  attach- 
ment, it  will  serve  to  register  synchronously  the  radial  beat  and  one 
other  pulsating  area,  such  as  the  jugular  vein,  the  cardiac  apex,  or 
an  aneurism.  Mackenzie's  ink  polygraph2  traces  three  separate 
records  upon  a  strip  of  white  paper. 

Jaquet's  sphygmocardiograph  (Fig.  12)  is  provided  with  a  small 
metal  plate  which  rests  upon  the  subject's  radial  artery,  and  is 


Fig.  12. — Jaquet's  sphygmocardiograpti. 

attached  to  a  delicate  lever  system  carrying  at  its  free  end  a  light 
stilet  for  registering  the  movements  of  the  radial  pulse;  a  second 
stilet  and  lever  system  plays  upon  a  tambour  on  the  instrument, 
and  leads,  by  a  rubber  tube,  to  a  special  receiver  designed  for  the 
cardiac  apex  (or  other  surface  pulsation),  being  adjusted  thereto 
by  a  chest-strap;  a  third  registering  mechanism, of  similar  construc- 
tion, communicates  with  a  cup-shaped  receiver  used  for  transmit- 

1  Price,  $20.00,  duty  paid  (T.  Hawksley;  also  J.  J.  Hicks,  London).  Biggs's 
time-marker,  registering  one-fifth  second  intervals,  and  designed  for  attach- 
ment to  Dudgeon's  sphygmograph,  is  furnished,  at  a  cost  of  $9.00,  by  Messrs. 
G.  Horstmann  and  Sons,  Bath,  England. 

1  Price,  $84.00,  duty  paid  (S.  Shaw,  Padiham,  England). 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION      39 

ting  the  jugular  impulse.  The  three  stilets  simultaneously  register 
upon  a  strip  of  smoked  paper,  which,  by  means  of  a  roller  and 
guide  wheels  revolved  by  clockwork,  travels  past  the  writing 
points  so  as  to  register  their  oscillations,  definite  time  intervals 
meanwhile  being  marked  by  a  chronograph  stilet.  The  driving 
and  time-marking  mechanisms  are  controlled  by  levers,  and  the 
pressure  of  the  radial  plate  is  regulated  by  a  milled  screw. 

Having  fitted  the  cardiac  receiver  to  the  apex-beat  and  strapped 
the  frame  of  the  instrument  snugly  to  the  patient's  wrist,  as  shown 
by  the  illustration  (Fig.  12),  the  leather  cuff  is  adjusted  so  as  to 
bring  the  metal  plate  beneath  the  frame  directly  over  the  radial 
pulse-beat,  the  site  of  which  has  been  previously  marked  with  an 
anilin  pencil.  The  smoked  paper  is  then  inserted  between  the  roller 
and  guide  wheels,  and  the  clockwork  started  in  order  to  carry  the 
strip  along  until  the  three  stilets  rest  upon  its  surface,  when  its  prog- 
ress is  halted.  The  cardiac  receiver  is  connected  with  its  appropriate 
tambour,  and  the  jugular  receiver  placed  in  position  and  similarly 
coupled  to  the  instrument.  When  the  three  stilets  rise  and  fall  with 
proper  amplitude,  indicating  satisfactory  registry  of  the  different 
undulations,  the  operator  starts  the  chronograph  and  again  sets  the 
paper  strip  in  motion  and  allows  it  to  run  its  entire  length,  while  an 
assistant  catches  the  tracing  as  it  passes  from  the  roller  and  guide 
wheels,  so  that  it  emerges  smoothly  and  evenly  from  the  instrument. 
Having  finished  the  tracing,  the  driving  power  is  stopped  and  the 
strip  benzoinated  or  varnished,  as  described  above. 

Dudgeon's  sphymograph,ior  tracing  the  radial  pulse- waves,  is  pro- 
vided with  a  single  lever  mechanism  similar  to  the  corresponding 
arm  of  the  sphygmocardiograph,f  or  which,  indeed,  Dudgeon's  device 
served  as  a  model  to  be  elaborated  by  the  incorporation  of  additional 
stilets,  receivers,  and  a  chronograph.  The  accompanying  picture 
(Fig.  13)  shows  the  correct  adjustment  of  the  sphygmograph,  held 
in  position  by  a  band  and  clamp,  so  that  the  metal  plate  of  the  register- 
ing lever  presses  upon  the  exact  point  where  the  radial  artery  beats 
most  forcibly.  Substitution  of  the  standard  metal  plate  by  a  slightly 
larger  one  attached  to  a  more  resilient  spring  has  given,  in  the  author's 
hands,  much  more  satisfactory  tracings  than  can  be  obtained  with  the 
original  model  of  the  instrument.  It  also  simplifies  the  technic  to 
tie  the  sphygmograph  to  the  wrist  with  a  flat  elastic  band,  as  Mac- 
kenzie advises,  rather  than  to  attempt  to  hold  it  in  place  by  means 
of  the  orthodox  strap  and  clamp.  Glover  uses  an  ordinary  tourni- 
quet fitted  with  a  cloth  band,  to  each  free  end  of  which  is  sewed 
a  metal  clip,  to  be  inserted  into  the  slots  where  the  wrist-bands  are 


40  PHYSICAL   DIAGNOSIS 

attached  in  the  original  model.  Having  adjusted  the  instru- 
ment so  as  to  establish  correct  oscillations  of  the  stilet,  the  smoked 
paper  strip  is  set  in  motion  and  the  tracing  completed  in  the  manner 
noted  above.1  While  this  is  taking  place  the  patient's  forearm 
should  rest  upon  a  firm  table,  being  supported  by  folded  towels  or 
similar  pads  so  placed  that  the  limb  is  kept  relaxed  and  immobile, 
while  the  fingers,  held  in  a  position  of  moderate  flexion,  likewise  must 
be  kept  perfectly  still. 


Fig.  13. — Dudgeon's  sphygmograph. 

Interpretation    of    the    Normal   Sphygmocardiogram. — The 

above  diagram  (Fig.  14)  illustrates  the  normal  undulations  recorded 
by  a  simultaneous  tracing  of  the  pulsations  of  the  carotid  artery,  the 
cardiac  apex,  and  the  right  external  jugular  vein,  the  synchronous 
points  on  these  three  waves  being  marked  by  the  numbered 
ordinate  lines. 

The  arterial  sphygmogram,  typified  by  the  carotid  tracing,  shows 
an  almost  perpendicular  upstroke  (3) ,  due  to  a  sudden  rise  of  blood- 
pressure,  followed  by  an  oblique  downstroke  (4-5) ,  corresponding  to 
the  fall  of  pressure.  A  line  drawn  through  the  lowest  points  of 
the  upstrokes,  termed  the  base  line,  normally  follows  a  virtually 
horizontal  course.  The  upstroke  (anacrotic  limb)  is  coincident 
with  ventricular  systole,  the  pulse-wave  arising  therefrom  being  so 
sharp  and  abrupt  that  it  produces  a  continuous  and  almost  vertical 

1  Tracings  in  ink  on  white  paper  can  be  made  by  fitting  the  Dudgeon  stilet 
with  Macfie's  glass  writing  point,  made  by  Messrs.  Down  Bros.,  21  St.  Thomas's 
Street,  London. 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       41 

line  on  the  sphygmogram.  The  downstroke  (catacrotic  limb)  is 
much  more  oblique,  for  it  mirrors  the  comparatively  slow  fall  of  blood- 
pressure,  and  this  line  shows  two  distinct  undulations:  one  known 
as  the  tidal  (predicrotic)  wave  (4),  due  to  secondary  contraction 
and  expansion  of  the  artery  immediately  after  its  systolic  distention; 
and  a  second,  termed  the  recoil  (dicrotic)  wave  (5),  caused  by  the 
recoil  of  the  blood-column,  whose  retreat  aortaward  is  suddenly 


12 


Fig.  14. — Simultaneous  tracings  of  the  normal  arterial,  venous,  and  cardiac  pulsa- 
tions (Sphygmocardiogram  by  Dr.  G.  Bachmann). 

checked  by  the  closure  of  the  aortic  valve.  Apart  from  these  two 
normal  oscillations  of  the  downstroke,  this  line  may  also  show  minia- 
ture waves  referable  to  the  inherent  elasticity  of  the  arterial  wall. 
The  apex  of  the  normal  arterial  tracing,  or  the  angle  between  the 
upstroke  and  the  downstroke,  is  acute,  while  of  the  two  minor 
downstroke  waves,  the  recoil  is  more  conspicuous  than  the  tidal. 

The  cardiogram,  shown  by  the  above  tracing,  consists  fundamen- 
tally of  a  perpendicular  upstroke  (2-3)  and  an  oblique  downstroke 
(5).  The  former  marks  the  beginning  of  ventricular  systole,  and 
may  be  preceded  by  a  minor  wave,  due  to  systole  of  the  left  auri- 
cle; ordinarily,  the  cardiogram  fails  to  show  this  auricular  undula- 
tion, the  immediately  preceding  diastolic  phase  of  which  is  difficult, 
if  not  impossible,  to  register  in  finer  detail.  The  summit  beyond 


42  PHYSICAL   DIAGNOSIS 

the  apex  (3)  is  known  as  the  systolic  plateau,  and  is  formed  by  a 
gently  sloping  line,  usually  rippled  by  one  or  more  subsidiary  waves, 
due  to  ventricular  contractions.  Chronologically,  the  systolic  plateau 
corresponds  to  the  impact  of  the  heart  against  the  parietes  during 
ventricular  systole,  and  from  this  summit  the  downstroke  drops,  with 
moderate  obliquity,  to  the  base  line.  The  curve  rising  immediately 
after  the  downstroke  (5)  coincides  with  ventricular  diastole,  the  first 
part  of  this  line  timing  the  active,  and  the  latter  part  the  passive, 
period  of  this  phase,  which,  graphically,  is  the  actual  beginning  of 
the  upstroke. 

The  venous  sphygmogram,  illustrated  by  the  jugular  tracing,  is 
composed  of  three  distinct  waves  corresponding  to  various  move- 
ments of  the  right  side  of  the  heart,  and  constituting  the  so-called 
"physiologic  venous  pulse."  The  first  of  these  waves  (a),  the 
auricular  or  a-wave,  is  presystolic  in  time,  being  coincident  with  the 
contraction  of  the  auricles,  and  is  due  to  the  centrifugal  impact  of  the 
venous  column  consequent  to  the  slowing  and  sudden  arrest  of  its 
onward  flow.  The  second  wave  (s),  commonly  termed  the  systolic, 
is  synchronous  with  the  beginning  of  ventricular  systole,  or  with  the 
so-called  " protosystolic  period"  of  this  chamber,  when  the  tricuspid 
valve  suddenly  projects  into  the  cavity  of  the  right  auricle  and  thus 
creates  a  reverse  wave  in  the  veins.1  The  third  wave  (v),  known 
as  the  ventricular,  is  also  systolic  in  time,  but  it  occurs  distinctly 
later  than  its  protosystolic  predecessor,  for  it  accompanies  the  latter 
phase  of  ventricular  contraction.  The  peculiar  double  curve  of  this 
undulation  is  produced  by  the  sudden  upward  movement  of  the  tri- 
cuspid valve  and  by  the  ascent  of  the  auriculoventricular  diaphragm 
to  its  resting  position — events  consequent  to  the  relaxation  of  the 
papillary  muscles  at  that  period  when  the  intraventricular  tension 
exceeds  the  intra-auricular.  The  notch  after  the  a-wave  (2)  marks 
relaxation  of  the  auricle;  that  following  the  s-wave  (Af)  indicates 
auricular  diastole;  and  that  succeeding  the  v-wave  (Vf)  designates 
ventricular  diastole  and  the  passive  period  of  the  cardiac  cycle. 

Clinical  Value  of  Sphygmocardiography. — Accurate  technic 
and  intelligent  interpretation  of  the  tracing  together  make  this 

1  Mackenzie  and  his  school  term  this  second  ascent  (s)  the  "  carotid  wave," 
and  attribute  it  to  the  communicated  impact  of  the  carotid  artery.  While  ad- 
mitting that  this  may  be  one  of  the  factors  of  the  s-wave,  the  arterial  impact 
cannot  be  the  sole  cause.  The  s-wave  unquestionably  precedes  the  systolic 
line  of  the  carotid  pulse  in  the  majority  of  accurate  kymograms ;  it  has  been 
repeatedly  traced  under  circumstances  absolutely  precluding  every  possibility 
of  a  transmitted  arterial  throb  (Bard,  Cushny,  Morrow);  and,  moreover,  its 
disappearance  has  been  noted  after  experimental  inhibition  of  the  ventricle 
(Porter). 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       43 

method  of  unquestionable  value,  the  all-important  personal  equation 
receiving,  of  course,  due  consideration  in  the  individual  instance. 
To  regard  sphygmocardiography  as  a  pleasing  bedside  pastime  is 
perhaps  as  great  an  error  as  to  expect  a  ready-made  diagnosis  from 
every  smoked  slip.  The  arterial  pulse  tracing  neither  can  nor  should 
supplant  the  trained  finger  in  studying  the  size,  volume,  and  mural 
condition  of  the  vessel,  but  it  does  provide  a  permanent  record  of  the 
pulse's  rate,  force,  and  rhythm,  which  thus  can  be  crystallized  on  a 
single  slip  of  blackened  paper,  together  with  numerous  minor  oscilla- 
tions too  delicate  to  be  felt.  Simultaneous  tracings  (i.  e.,  carotid, 
jugular,  and  precordial)  indicate,  as  no  other  method  of  research  can, 
disturbances  of  the  auriculoventricular  relations,  asynchronism  of 
ventricular  contraction,  and  other  cardiac  arhythmias  for  the  diagno- 
sis of  which  a  comparable  sphygmogram  is  indispensable. 

The  characteristics  of  individual  pulse  tracings  and  their  diagnostic 
significance  in  certain  cardiovascular  disorders  are  detailed  in  Sections 
V.  and  VI. 

ELECTROCARDIOGRAPHY 

With  the  electrocardiograph  it  is  possible  to  study  graphically 
the  electric  currents  generated  by  the  contracting  heart,  and  thus 
to  identify  with  great  accuracy  certain  cardiac  irregularities, 
notably  those  due  to  defects  of  conductivity,  to  premature  systoles 
of  the  auricles  and  ventricles,  to  sinus  disorders,  and  to  paroxys- 
mal tachycardia. 

The  electrocardiograph  now  in  general  use  was  perfected  by 
Einthoven,  on  lines  originated  by  Kolliker  and  Miiller,  in  1856, 
and  consists  essentially  of  a  delicate  filament  of  silvered  quartz 
stretching  between  the  poles  of  an  electromagnet  activated  by  a 
storage-battery  and  wired  to  electrodes  attached  to  the  subject.1 
The  current  traversing  this  filament  at  right  angles  to  the  lines 
of  force  of  the  electromagnet's  magnetic  field  deflects  it  according 
to  the  direction  of  the  current.  The  shadows  of  these  oscillations 
obtained  by  illumination  with  an  arc  light  and  magnified  by  a 
Zeiss  objective  and  a  system  of  condensing  lenses  are  focussed 
upon  a  photographic  film,  driven  at  fixed  speed,  which,  after 
proper  development,  constitutes  the  clinical  electrocardiogram. 
The  delicate  movements  of  the  filament  attributable  to  "skin 

1  The  duty-free  price  of  the  Edelmann  electrocardiographic  outfit  with  the 
Einthoven  string  galvanometer,  electrodes,  illuminating  system,  photographic 
registering  apparatus,  and  other  accessories  is  $1031;  the  Cambridge  instru- 
ment, complete,  costs  $1611,  duty  free.  (A.  H.  Thomas  Co.,  Philadelphia.) 


44 


PHYSICAL   DIAGNOSIS 


currents"  are  compensated  by  projecting,  by  means  of  a  rheostat, 
sufficient  current  from  a  dry  cell  exactly  to  neutralize  such  de- 
flections, and  the  tension  and  sensitiveness  of  the  filament  are  also 
adjustable,  usually  so  as  to  secure  a  lo-millimeter  deflection  with 
the  passage  of  a  i -millivolt  current. 

The  patient,  who  must  be  warm,  relaxed,  and  absolutely  at 
rest,  is  included  in  the  electric  circuit  by  electrodes  commonly 
consisting  of  zinc  vessels  containing  warm  salt  solution  in  which 
the  extremities  are  immersed,  or  of  strips  of  metal  enveloped  in 


Fig.  15. — Cambridge  electrocardiographic  outfit. 


absorbent  material  saturated  with  saline  and  applied  to  both 
arms  and  one  leg  of  the  subject.  The  course  of  the  current  thus 
led  off  is  termed  a  "lead,"  or  "derivation,"  designated  by  the 
Roman  numerals  I,  II,  III,  etc.,  according  to  the  parts  of  the 
patient  to  which  the  electrodes  are  attached.  Kraus  and  Nicoli 
have  plotted  six  different  leads,  all  of  which  afford  different  elec- 
trocardiograms, but  for  clinical  purposes  only  three  are  in  general 
use,  as  follows:  Lead  I,  current  from  right  arm  and  left  arm; 
lead  II,  current  from  right  arm  and  left  leg;  and  lead  III,  current 
from  left  arm  and  left  leg.  Lead  II  gives  the  most  useful  record 
in  the  majority  of  electrocardiograms  (Fig.  i6b). 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       45 

Interpretation  of  all  of  the  electrocardiographic  waves  is  still 
an  unsettled  point,  but  the  correctness  of  Einthoven's  conclusions 
as  to  the  conspicuous  deflections  is  generally  conceded.  These 
waves,  with  his  letterings,  represent  auricular  systole  at  P,  ven- 
tricular systole  at  Q,  R,  S,  T,  the  conduction  of  the  auriculo- 
ventricular  impulse  from  P  to  R,  and  the  diastolic  period  between 
T  and  P  (Fig.  160). 

By  means  of  these  simple  alphabetic  symbols  the  following 
pathologic  variations  of  sequence,  size,  and  incidence  of  the 


Fig.  16.— Lewis's  diagram  of  the  string  galvanometer:  A,  Microscope  for  observ- 
ing the  movements  of  the  string  of  silvered  quartz  (C)  suspended  in  the  field  of  the 
electromagnets  (S  N);  a,  direction  of  current's  movements,  at  right  angles  to  the  mag- 
netic field;  C  F,  electric  light  and  condenser. 

principal  waves  of  lead  II  of  the  electrocardiogram  may  be 
designated: 

1.  Irregular  incidence,  but  normal  sequence,  of  waves:  tachy- 
cardia; sinus  arhythmia. 

2.  Prolonged  P-R  interval:  sluggish  impulse  conduction  from 
sino-auricular  node  to  ventricle. 

3.  Prolonged  Q-R-S   complex:    delayed    impulse    conduction 
through  ventricle. 

4.  Replacement  of  P-wave  by  fine  oscillations:  auricular  fibril- 
lation. 

5.  Multiple  P- waves  in  R-T  interval:  auricular  flutter. 


46 


PHYSICAL   DIAGNOSIS 


6.  Small  or  inverted  P-wave,  with  premature  P-,  R-,  and  T- 
waves:  auricular  premature  systole. 

7.  Large  P-wave:  auricular  hypertrophy;  left  ventricular  dila- 
tation. 


Fig.  ioa. — Diagram  of  the  normal  electrocardiogram:  P,  Auricular  systole;  P-R, 
conduction-time  of  impulse  from  auricle  to  ventricle  (0.12  to  0.17  second);  Q,  beginning 
of  ventricular  systole;  R,  basal  ventricular  activity;  5,  apical  ventricular  activity;  T, 
end  of  ventricular  systole;  T-R,  diastolic  period. 

8.  Large  prolonged  /?-wave,  with  deep  5  depression :  ventricu- 
lar premature  systole.  (.ft-wave  inverted  in  lead  III,  if  left- 
sided,  and  in  lead  I,  if  right-sided.) 


in: 


Fig.  iot. — Normal  electrocardiogram.    Leads  I,  II,  and  III  of  a  normal  heart. 

9.  Small  .ft -wave:  ventricular  hypertrophy.    (/?-wave  inverted 
in  lead  III,  if  left-sided,  and  in  lead  I,  if  right-sided.) 

10.  Simple  inversion  of  /?-wave:  deep,  forced  inspiratory  effort; 
subphrenic  pressure. 


METHODS    AND    TECHNIC    OF   PHYSICAL    EXAMINATION      47 

11.  Small  R-\\3.ve:  cardiac  dilatation  (inconstant). 

12.  Large  T-wave:  vigorous  ventricular  contraction. 

13.  Small  or  inverted  T-wave:  feeble  ventricular  contraction. 
The  diagnostic  value  of  the  more  specialized  electrocardiograms 

in  various  lesions  of  the  myocardium  and  of  the  cardiac  valves 
is  duly  considered  in  Section  VI  (p.  396  et  seq.) . 


PARACENTESIS 

Pathologic  fluids  and  other  material  for  laboratory  study  are 
obtained  by  puncture,  or  paracentesis,  made  with  a  hollow  needle  or 
a  small  trocar,  ordinarily  attached  to  a  small  syringe  or  connected 
with  a  vacuum  bottle,  by  means  of  which  the  specimen  can  be  readily 
aspirated.  It  is  a  good  rule  always  to  be  prepared,  when  the  occasion 
arises,  to  remove  a  foreign  fluid  as  soon  as  it  is  detected,  so  as  to  spare 
the  patient  a  subsequent  operation.  In  consequence,  exploratory 
punctures,  though  primarily  diagnostic,  are  likewise  potentially 
curative.  In  this  manner  pathologic  fluids  within  the  pleura,  peri- 
cardium, and  peritoneum,  as  well  as  the  contents  of  cysts  and 
abscesses,  maybe  evacuated;  the  spinal  canal  tapped;  the  spleen 
and  liver  explored;  and  occasionally  the  consistence  and  nature  of 
obscure  tumors  determined. 

Technic. — Paracentesis  must  be  carried  out  under  rigid  asepsis, 
the  field  of  operation  being  scrubbed  with  a  i  :  1000  mercuric  chlorid 
solution,  cleaned  with  soap-suds,  rubbed  with  alcohol,  and  finally 
douched  with  sterile  water,  after  which  a  sterile  dressing  is  applied 
and  allowed  to  remain  in  place  until  the  time  of  the  puncture.  The 
needle,  syringe,  and  other  apparatus  are  to  be  sterilized,  prefer- 
ably by  boiling,  and  the  operator's  hands  must  be  surgically 
clean. 

The  site  of  puncture  having  been  chosen  (v.  i.),  the  needle  is 
introduced  steadily  but  rapidly,  and  without  any  boring  or  lateral 
twist,  until  a  sensation  of  suddenly  diminished  resistance  and  free 
mobility  is  perceptible,  indicating  that  the  point  has  passed  through 
the  parietal  structures.  To  prevent  damage  from  too  deep  a  punc- 
ture, the  operator  should  grasp  the  needle  with  the  thumb  and  fore- 
finger just  above  its  point,  while  piercing  the  comparatively  resistant 
tissues  of  the  surface.  After  withdrawal  of  the  needle  the  wcund 
is  dried,  covered  with  a  bit  of  sterile  gauze  or  cotton,  and  sealed  with 
aristol-collodion.  Only  exceptionally,  as  noted  below,  is  general 
anesthesia  indicated,  local  anesthesia  by  ethyl  chlorid  or  by  eucain 
being  usually  sufficient  to  deaden  the  pain  of  the  puncture. 


48 


PHYSICAL    DIAGNOSIS 


For  withdrawing  a  small  amount  of  fluid  it  is  best  to  use  an  explor- 
ing syringe  of  about  6  c.c.  capacity,  fitted  by  a  length  of  flexible 
rubber  tubing  to  a  hollow  needle,  the  length  and  caliber  of  which  are 
regulated  by  the  situation  and  nature  of  the  lesion  to  be  explored 
(Fig.  17).  For  routine  work  it  is  well  to  have  needles  of  three 
different  sizes:  56,  45,  and  30  gage,  and  2$  inches  (6.2  cm.),  3 
inches  (7.5  cm.),  and  3$  inches  (8.7  cm.)  in  length,  respectively.  In 
lieu  of  a  special  aspirator,  an  ordinary  hypodermic  needle  may 
sometimes  be  employed  with  success. 

When  considerable  fluid  is  to  be  removed,  it  may  be  allowed  to 
drain  off  spontaneously  through  a  coarse  hollow  needle  or  cannula 
(30  to  36  gage),  or  aspirated  into  a  vacuum  bottle.  For  aspirating 
a  large  effusion  most  clinicians  use  Potain's  apparatus,  consisting 
of  a  set  of  three  hollow  needles,  a  trocar-cannula,  and  a  graduated 
vacuum  bottle  and  exhaust  pump  (Fig.  18).  To  the  bottle  are 
fitted  two  rubber  tubes,  each  having  a  separate  stop-cock,  one  tube 
leading  to  an  aspirating  needle  and  the  other  to  the  pump,  used  to 
create  a  partial  vacuum  within  the  bottle  and  thus  to  exert  suction 
through  the  hollow  needle.  The  latter,  having  been  inserted  to  the 
proper^depth,  is  connected  with  the  aspirating  bottle,  from  which 
most  of  the  air  has  been  pumped  out,  the  vacuum  thus  created  being 
maintained  by  the  closure  of  both  stop-cocks.  Suction  is  established 
by  opening  the  needle  stop-cock  (the  pump-cock  remaining  closed) 


(Nt» 


Fig.  17. — Aspiration  syringe  and  needles. 

just  sufficiently  to  start  a  slow  flow  of  liquid  into  the  bottle.  If  it  be 
necessary  to  interrupt  the  aspiration  for  the  purpose  of  decanting 
the  fluid  and  reexhausting  the  air  within  the  bottle,  the  needle-cock 
must  remain  closed  meanwhile.  Failure  to  insert  the  needle  to  a 
sufficient  depth  commonly  accounts  for  a  "dry  tap,"  the  remedy 
for  which  is  obvious,  while  a  sluggish,  intermittent  flow  may  be  due 


METHODS    AND    TECHNIC    OF    PHYSICAL   EXAMINATION      49 

to  blocking  of  the  needle's  lumen  by  a  flake  of  fibrin,  to  unusual 
thickness  and  viscidity  of  the  exudate,  or  to  feeble  aspiration  force. 
These  last  obstacles  can  generally  be  overcome  by  reinserting  the 
needle  in  a  different  direction  after  having  partly  withdrawn  it  and 
cleared  its  bore  with  a  sterile  wire,  by  the  use  of  a  needle  of  larger 
caliber,  or  by  exhausting  more  air  from  the  bottle.  Having  finished 
the  aspiration  and  measured  the  fluid  withdrawn,  a  portion  for  subse- 
quent examination  is  poured  into  a  sterile  container,  or  the  vacuum 
bottle  itself  is  taken  directly  to  the  laboratory. 


Fig.  18. — Potain's  aspirator. 

The  laboratory  report  should  embody  data  relating  to  the  following 
points:  (a)  The  physical  properties  of  the  fluid — specific  gravity, 
color,  odor,  transparency,  consistence,  coagulability,  and  amount 
of  sediment;  (b)  chemic  examination  of  the  filtrate,  including  tests 
for  albumin,  serum-globulin,  and  mucin;  for  sugar  and  urea;  and, 
occasionally,  for  sarcolactic  acid,  succinic  acid,  allantoin,  and  inosite; 
(c)  microscopic  examination,  for  the  detection  of  blood-corpuscles, 
epithelial  and  endothelial  cells,  crystals,  necrotic  tissue,  ray  fungi, 
hydatid  booklets  and  membrane,  trypanosomes,  piroplasmas,  ame- 
bas,  and  pathogenic  bacteria,  which,  if  not  demonstrable  by  direct 
examination,  may  be  identified  by  culture  and  by  animal  inocula- 


50  PHYSICAL   DIAGNOSIS 

tion ;  (d)  cytodiagnosis ,  whereby  the  number  and  character  of  the  cells 
in  the  fluid  are  determined.  For  the  technical  details  of  these 
procedures  the  reader  should  consult  a  treatise  on  clinical  laboratory 
methods. 

Pleurocentesis. — Puncture  of  the  pleural  cavity  usually  calls 
for  the  use  of  a  rather  coarse  needle  and  a  Potain  aspirator,  for  in 
the  majority  of  instances  this  operation  is  a  curative  measure,  neces- 
sitating the  removal  of  much  fluid.  The  site  of  puncture  is  deter- 
mined by  the  size  of  the  effusion,  and  should  lie  well  below  the  upper 
level  of  the  fluid.  The  sixth  interspace  in  the  anterior  axillary  line, 


Fig.  i8a. — Pleurocentesis. 

the  seventh  interspace  in  the  midaxillary  line,  and  the  eighth  inter- 
space midway  between  the  latter  and  the  scapular  line  are  the  points 
of  election  suitable  in  most  effusions  of  average  extent  (Fig.  19). 
Too  high  a  puncture  may  lacerate  the  lung  above  the  effusion,  while 
if  the  needle  be  inserted  at  too  low  a  level,  it  may  penetrate  the  com- 
plementary pleural  space,  or  tear  the  diaphragm,  the  liver,  or  the 
spleen. 

If  possible,  the  patient,  who  must  limit  respiratory  excursions, 
should  sit  upright  during  the  operation,  with  the  arm  of  the  affected 
side  swung  across  the  chest  so  that  the  hand  rests  upon  the  oppo- 
site shoulder,  thus  widening  the  intercostal  spaces.  The  puncture 
site  having  been  chosen,  the  needle  should  be  thrust  directly  through 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       51 


the  middle  of  the  proper  interspace,  thus  avoiding  the  possibility 
of  wounding  an  intercostal  artery  and  of  lacerating  the  costal  peri- 
ostium.  The  effusion  must  be  aspirated  slowly,  for  its  sudden  with- 
drawal is  not  unattended  by  risk,  chiefly  from  the  sudden  recession 
of  the  dislocated  heart  and  from  abrupt  refilling  of  the  previously 


Pericardium 


Peritoneum 


Pericardium 


Pleura 


Peritoneum 


Fig.    19. — Points  of  election  for  paracentesis  of  the  thorax  and  abdomen. 

collapsed  blood-vessels  of  the  lung.  Aside  from  sealing  the  punc- 
ture wound,  the  affected  side  requires  no  attention,  for  it  seems 
better  to  permit  free  movement  of  the  thorax  than  to  restrict  it  by 
strapping,  as  was  formerly  considered  good  practice.  After  the 
patient  has  passed  three  or  four  days  in  bed  subsequent  to  the  para- 
centesis, it  is  advisable  to  hasten  expansion  of  the  deflated  lung  by 
means  of  respiratory  exercises.  This  is  accomplished  preferably 
by  the  use  of  a  Wolff  apparatus,  whereby  the  patient,  by  blowing 
a  measured  volume  of  water  alternately  from  one  bottle  into  another, 
exerts  a  respiratory  effort  against  a  given  degree  of  resistance. 

In  that  type  of  encysted  effusion  known  as  "  blocked  "  pleurisy 
(pleuresie  bloquee)  ordinary  aspiration  fails  to  liberate  the  fluid,  in 


52  PHYSICAL   DIAGNOSIS 

which  event  two  needles  may  be  used,  one  for  drainage  and  the 
other  for  forcing  sterile  air  into  the  pleural  pocket,  thus  driving  out 
the  contained  liquid. 

The  amount  of  fluid  to  be  withdrawn  at  one  sitting  depends  essen- 
tially upon  the  manner  in  which  the  subject  bears  the  aspiration; 
in  general,  however,  the  volume  should  be  too  little  rather  than  too 
great.  If  all  goes  well,  it  is  safe  slowly  to  drain  off  at  least  a  liter — 
if  this  much  exists — or,  in  the  case  of  a  massive  effusion,  as  much 
as  one  and  one-half  liters,  removing  the  remainder  a  day  or  two  later. 
If  the  patient  coughs,  gasps,  and  complains  of  pain  in  the  chest, 
faintness,  and  suffocation,  and  if  the  blood-pressure  falls  notably, 
the  aspiration  must  be  temporarily  suspended,  or,  if  these  symptoms 
persist,  permanently  abandoned,  at  least  for  the  time  being.  It 
is  not  always  necessary  to  aspirate  a  large  volume  of  intrapleural 
fluid,  for  the  withdrawal  of  a  small  amount  (10  to  20  c.c.)  may 
stimulate  absorption  sufficiently  to  dispose  of  the  remainder  by 
way  of  the  lymphatic  apparatus. 

Artificial  pneumothorax  is  a  remote  accident,  and  one  arising  only 
in  consequence  of  gross  carelessness — air  cannot  enter  the  pleura  if 
the  needle  and  bottle  be  properly  connected,  and  if  the  needle^  stop- 
cock be  opened  only  when  a  satisfactory  vacuum  exists  within  the 
bottle.  To  assure  this  last  essential  the  suction  power  and  the  valve 
action  of  the  bottle  should  always  be  tested  with  sterile  water  before 
using  the  instrument  of  the  patient.  Sudden  death  of  the  subject 
during  paracentesis,  a  most  unusual  accident,  has  been  referred  to 
extreme  inhibition  of  the  heart,  due  to  irritation  of  the  vagus  and 
to  vasomotor  and  respiratory  paralyses  from  grave  depression  of 
the  vasomotor  and  respiratory  centers. 

Capps  and  Lewis  have  drawn  attention  to  the  danger  of  exciting 
a  vasodilator  reflex  by  irritation  of  the  pleura,  in  consequence 
of  which  death  may  occur  after  a  period  of  rapid  and  extreme 
decline  of  arterial  tension,  attended  by  shallow  and  hurried  respira- 
tion and  by  other  symptoms  of  collapse.  Such  an  accident  should 
be  guarded  against  by  making  the  puncture  with  great  care  and 
by  avoiding  unnecessarily  deep  penetration  and  irritation  of  the 
pleura  with  the  needle;  the  emergency,  should  it  arise,  is  best 
treated  by  adrenalin  transfusion. 

A  form  of  autotoxemia  resembling  so-called  "serum  illness," 
and  characterized  by  albuminuria,  fever,  arthritis,  and  urticarial 
rashes,  is  a  very  remote  sequel  to  pleural  paracentesis.  Albuminous 
expectoration  also  may  follow  the  operation,  but  this  accident  need 
not  be  feared  if  the  fluid  has  been  drained  off  slowly  and  with  care. 


METHODS    AND   TECHNIC    OF   PHYSICAL   EXAMINATION      53 

Examination  of  a  pleural  fluid  has  for  its  chief  object  the  differ- 
entiation of  an  edematous  transudate  from  an  inflammatory  exu- 
date,  both  of  which  may  have  precisely  the  same  transparency  and 
yellowish  hue,  yet  within  certain  limits  are  distinguishable  by  differ- 
ences in  specific  gravity,  protein  content,  coagulability,  and  micro- 
scopic elements.  A  transudate,  which  resembles  lymph,  usually 
has  a  specific  gravity  of  1015  or  .lower,  contains  not  more  than  2.5 
per  cent,  of  albumin,  and,  unless  mixed  with  blood,  does  not  coagu- 
late spontaneously.  Microscopically,  it  shows  little  or  no  fibrin 
and  a  few  endothelial  cells  derived  from  the  pleural  wall;  blood- 
cells  are  found,  if  hemorrhage  coexists,  and  fat-droplets,  if  the  fluid 
be  chylous.  An  exudate  generally  shows  a  specific  gravity  of  1018 
or  higher,  contains  at  least  4  per  cent,  of  albumin,  and  clots  promptly 
and  completely.  Microscopically,  a  dense  fibrin  network  is  found, 
and  also  degenerated  endothelium,  leukocytes,  erythrocytes,  and 
perhaps  cholesterin  crystals;  pathogenic  bacteria  may  or  may  not  be 
demonstrable  in  the  stained  specimen,  according  to  the  nature  of 
the  underlying  inflammatory  process.  Although  difficult  to  apply 
clinically,  Zagoumenny's  rule  generally  holds  true,  viz.,  that  the 
alkalinity  of  exudates  is  less  than  that  of  the  patient's  blood,  while 
the  alkalinity  of  transudates  is  about  the  same  as  that  of  the  blood. 

Some  exudates  are  frankly  purulent  or  putrid,  and,  therefore, 
undeniably  of  inflammatory  and  infectious  origin;  some  are  hemor- 
rhagic,  in  which  case  either  a  tuberculous  or  a  cancerous  factor  may 
be  at  work;  some  are  eosinophilic,  as  in  tuberculosis,  rheumatic 
fever,  and  a  wide  variety  of  other  diseases;  and  some  are  milky  or 
opalescent,  for  which  peculiarities  the  presence  of  fat-droplets  or 
of  delicate  albumin  granules  may  account.  In  general  terms  it  is 
true  that  the  protein  content  of  both  dropsical  and  inflammatory 
fluids  largely  depends  upon  the  site  of  the  effusion,  and  is  higher, 
as  a  rule,  in  pleural  fluids  than  in  those  drawn  from  the  perito- 
neum. 

Cytodiagnosis  is  useful  principally  in  determining  the  nature  of  a 
bacteria-free  fluid,  and  is  based  upon  investigation  of  the  number 
and  character  of  the  cellular  elements  observed  in  a  stained  film  of 
the  effusion.  The  relative  proportions  of  lymphocytes  and  polynu- 
clear  leukocytes,  and  also  the  erythrocytes  and  the  cells  derived  from 
endothelial  surfaces  and  from  neoplasms,  serve  as  the  criteria  for 
deductions,  which  relate  chiefly  to  the  differentiation  of  tuberculous 
and  non-tuberculous  effusions. 

A  differential  count  showing  lymphocytosis,  or  a  predominance  of 
mononuclear  leukocytes,  suggests  either  a  mild  or  a  subsiding  inflam- 


54  PHYSICAL   DIAGNOSIS 

mation,  or  some  non-inflammatory  process.  Chronic  tuberculous 
exudates  are  thus  characterized,  save  during  their  incipiency  and 
when  active  inflammatory  complications  supervene,  under  which 
circumstances  the  polynuclears  are  unduly  numerous. 

A  count  affording  polynucleosis ,  or  a  preponderance  of  polynu- 
clear  leukocytes,  generally  denotes  a  well-defined  and  active 
inflammation  of  acute  infectious  origin,  due,  for  example,  to  strep- 
tococci, staphylococci,  pneumococci,  or  meningococci,  and  if  such 
a  process  be  of  striking  intensity,  there  will  possibly  be  many 
necrotic  cells  and  much  detritus. 

Endotheliocytosis,  by  which  is  meant  an  undue  relative  or  absolute 
increase  in  the  number  of  endothelial  cells,  is  the  general  rule  in 
non-inflammatory  transudates,  and  in  such  fluids  both  lymphocytes 
and  polynuclears,  particularly  the  latter,  are  in  the  minority. 

The  detection  of  cancer  cells,  many  with  mitotic  figures  therein, 
in  a  fluid  that  also  contains  small  bits  of  tissue  of  distinctively  can- 
cerous structure,  points  to  the  malignant  origin  of  the  effusion. 
Caution  must  be  observed,  in  the  absence  of  corroborative  cyto- 
logic  findings,  in  attempting  to  differentiate  true  cancer  cells  from 
endothelial  elements,  an  unnatural  number  of  which,  free  and  en 
plaque,  Sahli  speaks  of  finding  in  most  effusions  of  cancerous 
character. 

Inoscopy  may  demonstrate  tubercle  bacilli  in  an  effusion  giving 
negative  bacteriologic  findings  when  examined  by  ordinary  methods 
of  film-staining.  The  technic  of  inoscopy,  as  elaborated  by  Jousset, 
consists  of  digesting  the  coagulum  of  the  suspected  liquid  with  pepsin 
and  hydrochloric  acid,  centrifugalizing  the  liquefied  mass,  and 
preparing  films  from  the  sediment,  to  be  stained  by  the  Ziehl-Gabbet 
method  and  examined  microscopically. 

Pericardicentesis. — Puncture  of  the  pericardial  sac  is  not  to  be 
undertaken  lightly,  inasmuch  as  a  slight  technical  slip  may  irrepar- 
ably damage  the  heart;  but,  with  due  care,  the  operation  is 
practically  without  danger.  Curative  pericardicentesis  is  indis- 
pensable in  dealing  with  a  bulky  effusion  showing  no  tendency  to 
undergo  resorption,  and  in  a  condition  of  this  sort  the  physical  signs 
are  so  unmistakable  that  a  merely  diagnostic  puncture  is  neither 
indicated  nor  justified. 

With  the  subject  sitting  upright  or  semiprone  and  restricting 
respiratory  movements  as  much  as  possible,  the  needle  is  introduced 
through  the  middle  of  an  interspace  at  a  point  within  the  area  of 
cardiac  percussion  flatness.  The  instrument  is  then  pushed  inward 
along  a  horizontal  plane  while  piercing  the  muscle,  after  which  its 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION      55 

point  is  cautiously  directed  inward  until  a  sense  of  abolished  resist- 
ance marks  its  entrance  to  the  pericardial  sac.  Ordinarily,  the  fifth 
left  intercostal  space  between  the  midclavicular  line  and  the  ex- 
treme outer  limit  of  effusion  flatness  is  by  far  the  most  satisfactory 
site  for  puncture,  though  some  prefer  the  fourth  or  the  fifth  left 
interspace,  either  close  to  or  at  least  one  inch  (2.5  cm.)  from  the 
sternal  border,  so  as  to  clear  the  internal  mammary  artery,  which 
parallels  the  breast-bone  at  a  distance  of  from  £  to  £  inch  (0.6- 
1.25  cm.)  from  its  margin  (Fig.  19).  In  a  very  large  effusion 
the  freest  drainage  is  sometimes  secured  by  tapping  the  pericardium 
through  the  fourth  right  interspace  close  to  the  sternum  (Dobert), 
or  through  the  left  costoxiphoid  angle  (Osier),  thrusting  the  needle 
upward  and  backward  and  hugging  the  costal  margin. 

In  order  to  avoid  causing  sudden  relief  of  the  extracardial  pressure, 
the  fluid  must  be  drained  away  slowly  and  in  limited  amounts,  not 
more,  for  example,  than  3  or  4  ounces  (90-120  c.c.)  at  a  single  seance, 
which  may  have  to  be  repeated  subsequently  if  the  effusion  be  of 
considerable  volume.  The  wound  made  by  the  needle  requires 
no  attention  other  than  the  treatment  advised  above. 

Examination  of  the  pericardial  fluid,  by  the  methods  just 
alluded  to,  decides  the  type  of  the  effusion  in  question,  whether  it 
be  the  dropsical  serum  of  hydropericardium,  the  bloody  effusion 
of  hemopericardium,  the  milky  liquid  of  chylopericardium,  or  the 
inflammatory  exudate  of  pericarditis.  The  physical  properties  and 
other  characteristics  of  liquid  effusions  obtained  from  the  pericardial 
sac,  being  essentially  like  those  of  corresponding  pleural  liquids,  do 
not  require  separate  consideration  (v.  s.). 

Paracentesis  Abdominis. — Diagnostic  puncture  of  the  abdominal 
cavity  is  sometimes  indicated  in  the  investigation  of  abdominal  cyst, 
circumscribed  abscess,  and  solid  tumor,  and  under  such  circum- 
stances the  needle  virtually  fills  the  dual  office  of  instrumental  pal- 
pation and  aspiration.  Hydrcnephrosis,  subphrenic  abscess,  and 
cysts  of  the  ovary  and  pancreas  may  come  within  reach  of  the  explor- 
ing needle,  but  it  is  safer  to  cut  down  on  a  distended  gall-bladder 
than  to  attempt  its  puncture,  owing  to  the  tendency  of  bile  to 
escape  into  the  peritoneum  after  the  withdrawal  of  the  needle.  In 
making  the  puncture  the  operator  guides  the  instrument  so  that 
it  unquestionably  penetrates  the  mass  aimed  at,  and  in  this  attempt 
great  care  is  to  be  observed  to  prevent  peritoneal  contamination, 
either  through  a  breach  in  the  punctured  part,  or  by  leakage  of 
infected  material  from  the  eye  of  the  needle.  The  latter  is  used 
in  connection  with  an  aspiration  syringe,  and  should  be  of  small 


50  PHYSICAL   DIAGNOSIS 

caliber  (about  50  gage),  of  high  tensile  strength,  and  of  sufficient 
length  to  penetrate  deeply.  In  the  diagnosis  of  pneumoperito- 
neum  Herrick's  method  of  paracentesis  with  a  blunt  trocar  and 
laterally  perforated  cannula  is  good  practice.  The  cannula,  being 
connected  by  rubber  tubing  with  a  wash-bottle  containing  water, 
transfers  the  free  peritoneal  gas  to  the  liquid,  the  bubbling  of 
which  gives  an  ocular  proof  of  gas. 


Fig.  iga. — Paracentesis  abdominis.    Inserting  the  trocar  and  cannula. 

Therapeutic  puncture  of  the  peritoneal  cavity  for  the  relief  of 
ascites  is  usually  made  alongside  the  median  line  of  the  abdomen, 
at  a  point  midway  between  the  pubic  symphysis  and  the  umbilicus; 
or  at  Munro's  point,  midway  between  the  umbilicus  and  the  left 
anterior  superior  iliac  spine  (Fig.  19).  Inasmuch  as  the  deep  epi- 
gastric artery  lies  dangerously  close  to  the  latter  point,  Lian's  site 
of  election  for  puncture  (the  junction  of  the  outer  and  middle 
thirds  of  an  umbilico-iliac  line)  may  seem  a  safer  situation  for 


METHODS    AND    TECHNIC    OF   PHYSICAL    EXAMINATION      57 

introducing  the  trocar.  The  patient  should  be  placed  in  a  sitting 
posture,  or,  if  bed-ridden,  propped  up  in  a  semireclining  atti- 
tude, so  as  to  favor  gravitation  of  the  fluid  to  the  lowest  level 
of  the  peritoneal  cavity.  Having  found  that  the  subject's  bladder 
is  empty,  and  that  the  intestines  are  out  of  the  way,  a  sterile 
muslin  binder  is  fitted  snugly  around  the  abdomen,  by  which 
device  uniform  parietal  pressure  is  applied  while  the  fluid  is  es- 


Fig.  196. — Paracentesis  abdominis.     Fluid  draining  away,  with  trocar  withdrawn  and 

cannula  in  position. 

caping.  This  binder,  reaching  from  the  lower  epigastrium  to  the 
pubis,  should  be  provided  with  a  window  in  front  and  with  in- 
terlacing tails  behind,  the  former  corresponding  to  the  field  of 
operation  and  the  latter  being  used  for  traction.  The  punc- 
ture is  made  with  a  trocar  and  cannula,  the  former  being  withdrawn 
when  the  peritoneal  sac  is  entered,  and  the  fluid  allowed  to  flow 
through  the  tube  into  a  receptacle  beside  the  patient.  As  the  transu- 
date  drains  off,  commensurate  support  is  given  to  the  abdominal 


58  PHYSICAL   DIAGNOSIS 

wall  by  an  assistant  who  stands  behind  the  patient  and,  by  taking 
up  the  slack  of  the  interlacing  tails,  keeps  the  binder  tightly  applied 
to  the  abdomen  as  its  size  diminishes.  This  not  only  facilitates  the 
flow,  but  to  some  extent  wards  off  troublesome  syncope,  due  to  the 
sudden  rush  of  blood  from  the  periphery  to  the  overdilated,  toneless 
abdominal  vessels.  Syncope  from  too  rapid  withdrawal  of  the 
fluid  can  be  averted  by  the  use  of  a  cannula  of  proper  size  (about 
35  gage),  and  by  stopping  the  flow  with  the  finger,  from  time  to  time, 
should  the  patient  complain  of  vertigo  or  faintness.  An  apparently 
dry  abdomen  sometimes  still  yields  a  surprisingly  large  quantity  of 
fluid  when  the  point  of  the  cannula  is  directed  downward  and 
swept  about,  while  the  subject  bends  far  forward,  compresses  the 
abdomen  laterally  with  both  hands,  and  contracts  the  abdominal 
muscles.  After  the  cannula  is  removed  and  the  wound  sealed,  as 
above  directed,  a  tight  abdominal  binder  is  applied,  and  the  patient 
put  to  bed  for  about  twenty-four  hours. 

Buth's  method  of  gradual  evacuation  is  suitable  if  one  fears 
the  effects  of  the  pain  of  puncturing  with  a  large  trocar  or  the 
danger  of  shock  from  too  rapid  a  drainage  of  a  massive  effusion. 
This  calls  for  the  use  of  a  "capillary  trocar"  and  a  cannula  about 
f  inch  (8  cm.)  long  and  a  diameter  approximating  ^r  inch  (i \  mm.), 
with  lateral  perforations  near  the  end  introduced  into  the  peri- 
toneum and  with  a  bulbous  extremity  for  attaching  a  rubber  tube. 
The  instrument  having  been  introduced  in  the  usual  manner,  its 
point  is  directed  downward  through  the  belly  wall,  and  after 
withdrawing  the  trocar  and  fitting  a  length  of  drainage-tubing 
to  the  end  of  the  cannula,  the  fluid  is  allowed  to  drain  into  a 
receptacle  alongside  the  patient.  The  fluid,  which  if  fibrinous 
will  not  flow  at  all  through  such  a  small  cannula,  is  usually  evacu- 
ated at  the  rate  of  from  i  to  i\  quarts  (i  to  15  liters)  per  hour,  and 
with  a  minimum  of  discomfort  to  the  patient. 

Drainage  of  the  abdominal  cavity,  if  skilfully  done,  is  quite  with- 
out danger,  and  may  be  repeated  time  and  again  in  the  same  indi- 
vidual with  perfect  immunity  from  by-effects,  as  many  an  old  alco- 
holic with  a  hard  liver  can  testify.  Even  in  preantiseptic  days  the 
harmlessness  of  repeated  punctures  of  the  belly  was  recognized,  if 
one  may  judge  by  Algernon  Ashton's  description  of  a  century-old 
English  epitaph,  which  naively  sets  forth  that  the  deceased  "was 
tapped  97  times,  and  had  461  gallons  of  water  taken  from  her, 
without  ever  lamenting  her  case  or  fearing  the  operation." 

Examination  of  the  fluid  obtained  by  abdominal  puncture  aims 
to  distinguish  ascitic  transudates  from  peritoneal  exudates,  by  the 


METHODS    AND    TECHNIC    OF   PHYSICAL   EXAMINATION      59 

criteria  already  mentioned  (v.  s.),  and  to  identify  fluids  aspirated 
from  ovarian,  echinococcus,  hydronephrotic,  and,  rarely,  pancreatic 
cysts. 

Ovarian  cysts  have  a  most  variable  composition,  their  contained 
fluid  being  commonly  viscid  and  turbid  or  colloid,  but  excep- 
tionally resembling  a  thin,  watery  transudate.  The  specific  gravity 
ranges  from  about  1005  to  1050,  according  to  the  richness  of  the 
albumin  content,  and  the  color  may  be  amber,  greenish,  brightly 
sanguineous,  or  chocolate  brown.  The  cystic  fluid  is  of  alkaline 
reaction,  and  contains,  in  addition  to  albumin,  metalbumin,  the 
presence  of  which  is  believed  to  be  diagnostic.  In  a  questionable 
fluid  the  absence  of  fibrin  points  to  an  ovarian  cyst  rather  than 
to  ascites.  Urea  and  uric  acid  are  sometimes  found  in  considerable 
amount,  and  microscopic  examination  shows  blood-cells  and  blood- 
pigment,  degenerated  epithelium,  and  often  colloid  masses.  In 
an  ovarian  dermoid,  hairs,  squamous  epithelium,  fat,  and  choles- 
terin  are  the  significant  findings. 

Echinococcus  cysts  yield  a  clear  alkaline  fluid  having  a  specific 
gravity  usually  not  exceeding  1010,  and  containing  a  large  amount 
of  sodium  chlorid,  little  or  no  albumin,  a  variable  quantity  of  glu- 
cose, and,  sometimes,  inosite  and  succinic  acid.  The  foregoing 
composition  of  the  cyst  fluid  is  greatly  altered  should  it  be 
contaminated  by  pus  or  by  blood,  in  the  event  of  which  the 
diagnosis  must  be  made  entirely  with  the  microscope.  This 
shows  distinctive  echinococcus  scolices,  hooklets  derived  there- 
from, and  fragments  of  cyst  membrane,  with  such  minor  find- 
ings as  eosinophile  cells,  cholesterin  and  hematoidin  crystals,  and 
fatty  cells. 

Fluid  from  hydronephrotic  cysts,  if  uncontaminated,  may  be 
either  clear  and  watery,  or  amber  tinted  and  cloudy,  and  generally 
ranges  in  specific  gravity  from  about  1010  to  1015.  The  detection 
of  renal  epithelium  in  the  fluid  is  proof  positive  of  hydronephrosis, 
while  the  presence  of  a  considerable  amount  of  urea  and  uric  acid  is 
suggestive,  but  not  conclusive,  since  both  these  substances  are 
commonly  found  in  the  contents  of  ovarian  and  pancreatic  cysts, 
and  urea  is  demonstrable  in  both  inflammatory  and  mechanical 
effusions.  Apart  from  these  details,  there  is  nothing  to  be  learned 
from  the  microscopic  examination. 

From  a  pancreatic  cyst  of  recent  origin  and  rapid  development 
one  expects  to  obtain  an  alkaline  fluid  of  low  specific  gravity  and 
hemorrhagic  character,  containing  a  characteristic  tryptic  ferment, 
owing  to  the  presence  of  which  the  fluid,  despite  its  alkaline  reaction, 


60  PHYSICAL   DIAGNOSIS 

has  the  property  of  digesting  egg-albumen.  This  most  distinctive 
proof  of  a  pancreatic  fluid  is  supplemented  in  some  instances  by 
the  demonstration  of  diastatic  and  fat-splitting  ferments,  whose 
significance  is,  however,  in  nowise  pathognomonic.  In  an  old  cyst 
the  tryptic  ferment  is  rarely  obtained,  for  it  tends  to  disappear 
as  the  lesion  ages.  Albumin,  uric  acid  and  urates,  cholesterin, 
and  blood-pigment  are  other  common  constituents  of  cysts  of  the 
pancreas. 

Lumbar  Puncture. — This  procedure,  popularized  by  Quincke, 
consists  of  tapping  the  subarachnoid  space  below  the  termination  of 
the  spinal  cord,  with  the  dual  object,  diagnostically,  of  obtaining  a 
sample  of  cerebrospinal  fluid  for  examination  and  of  determining 


: 

Fig.  igc. — Lumbar  puncture.    Inserting  the  needle  in  the  fourth  lumbar  interspace. 

the  degree  of  intraspinal  pressure.  Therapeutically,  lumbar  punc- 
ture is  a  means  of  relieving  undue  cerebrospinal  tension,  of  draining 
the  spinal  canal  and  irrigating  it  locally,  of  administering  meningitis 
serum  and  salvarsanized  blood-serum,  and  of  producing  spinal 
anesthesia.  The  puncture  may  be  made  either  with  a  stilet 
needle  devised  for  the  purpose,  or  with  an  ordinary  hollow  needle 
of  about  45  gage  and  three  or  four  inches  (7.5  to  10  cm.)  in 
length. 

The  patient  is  placed  in  lateral  decubitus,  back  toward  the  opera- 
tor, with  thighs  flexed  upon  the  abdomen  and  trunk  bent  well  for- 
ward so  as  to  widen  the  intervertebral  spaces.  Or  the  patient 
may  sit  facing  the  back  of  a  chair,  with  the  trunk  arched  passively 
forward  and  the  arms  and  legs  relaxed.  General  anesthesia 


6i 

is  usually  indicated  in  young  children,  but  in  adults  it  is  unneces- 
sary. By  preference  the  puncture  is  made  between  the  spines  of 
the  fourth  and  fifth  lumbar  vertebrae,  for  here  the  spinal  cord, 
terminating  at  the  level  of  the  second  lumbar  vertebra,  cannot  be 
lacerated.  The  fourth  lumbar  interspace  is  crossed  by  a  horizontal 
line  connecting  the  highest  points  of  the  two  iliac  crests.  At  this 
level  and  at  a  point  about  one-half  inch  (1.25  cm.)  to  one  side  of  the 
midspinal  line  the  needle  is  thrust  through  the  skin  and  cautiously 
pushed  upward  and  inward  until  it  enters  the  spinal  canal,  at  a  depth 
varying  from  about  £  inch  to  ij  inches  (2  to  4  cm.)  in  children,  to 
twice  these  distances  in  adults.  As  a  rule,  the  fluid  drips  from  the 


Fig.  IQ</. — Lumbar  puncture.     Collecting  the  cerebrospinal  fluid  after  paracentesis. 

needle  as  soon  as  the  point  enters  the  subarachnoid  space,  and  can 
be  collected  in  a  sterile  tube  as  it  flows  out^drop  by  drop.  If  aspira- 
tion be  necessary,  the  suction  must  be  very  slow  and  gentle,  for  fear 
of  mechanically  injuring  the  delicate  spinal  structures.  Danger  of 
damage  by  the  needle's  point  is  minimized  by  using  a  flexible  rubber 
coupling  between  the  mouth  of  the  needle  and  the  syringe.  A 
"dry  tap"  may  sometimes  be  made  productive  by  cautiously  with- 
drawing the  needle  a  short  distance  and  reinserting  it,  by  moving 
the  patient's  head  and  neck  backward  and  forward  and  straightening 
the  spine,  or  by  passing  a  sterile  wire  through  the  bore  of  the  needle 
to  dislodge  clots  and  fibrin  flakes  therein.  The  pressure  of  the 


02  PHYSICAL    DIAGNOSIS 

cerebrospinal  fluid  is  roughly  estimated  by  noting  the  velocity  with 
which  the  first  few  drops  escape  from  the  open  end  of  the  needle, 
hypotension  being  indicated  by  a  forceless  dribble,  and  hypertension 
by  a  streaming  forth,  of  the  fluid.  Deviations  from  the  normal  pres- 
sure (about  5  to  7  mm.  Hg.)  are  detected  accurately  by  a  small 
mercury  manometer.  When  the  operation  is  finished  and  the  needle 
withdrawn,  the  puncture  wound  is  dressed  with  sterile  gauze  or  sealed 
with  cotton  and  collodion,  and  the  patient  kept  in  bed  for  the 
ensuing  twenty-four  hours  or  longer. 

Normal  cerebrospinal  fluid,  of  which  from  5  to  10  c.c.  ordinarily 
can  be  withdrawn  by  lumbar  puncture,  is  an  alkaline  fluid  of  low 
specific  gravity  (1006  to  1008),  and  having  the  transparent,  limpid 
appearance  of  distilled  water,  or,  less  commonly,  being  of  a  faint 
yellowish  hue.  It  contains  a  small  amount  of  protein,  chiefly  in 
the  form  of  serum-globulin,  and  also  chlorids,  traces  of  urea  and 
cholin,  and  a  copper-reducing  substance  akin  to,  if  not  identical 
with,  glucose.  Microscopically,  an  occasional  endothelial  cell  and 
leukocyte,  and  often  numerous  erythrocytes,  derived  from  the  punc- 
ture, are  found. 

The  volume  of  the  fluid  is  generally  increased,  in  some  cases  even 
a  hundredfold,  and  its  flow  proportionately  accelerated,  in  menin- 
gitis, hydrocephalus,  intracranial  tumor,  paresis,  and  certain  infectious 
diseases.  It  may  be  blood  streaked  as  the  result  of  apoplexy,  turbid 
and  yellow  in  purulent  meningitis,  yellowish-green  in  jaundice,  and 
delicate  blue  after  the  administration  of  methylene-blue.  The 
specific  gravity  of  the  fluid  rises  decidedly  as  the  consequence  of 
meningeal  inflammation,  and  it  is  usually  higher  than  normal  in 
paretics.  The  chemic  composition  of  the  fluid  deviates  from  the 
normal  in  certain  disorders,  and,  in  general  terms,  such  variations 
are  of  diagnostic  utility.  The  protein  content,  which  tends  to  rise 
after  repeated  tappings,  may  also  be  excessive  in  lesions  responsible 
for  a  large  increase  in  the  cellular  elements  of  the  fluid,  but  it  cannot 
be  held  that  the  protein-cell  relation  is  always  constant  or  propor- 
tionate. Albumin  is  appreciably  increased  in  purulent  meningitis, 
paresis,  intracranial  tumor,  and  apoplexy.  An  undue  amount  of 
cholin  in  the  cerebrospinal  fluid  indicates  disintegration  of  nerve 
tissue,  and  in  general  paresis,  epilepsy,  multiple  sclerosis,  alcoholic 
neuritis,  and  beri-beri  this  product  of  decomposition  is  commonly 
encountered.  The  chlorids  are  diminished  in  uremia  (Carriere),  and 
in  this  intoxication  there  is  usually  an  increase  of  the  urea,  albumin, 
phosphates,  and  sulphates  of  the  fluid.  The  reducing  agent  nor- 
mally present  in  the  cerebrospinal  fluid  is  frequently  absent  hi 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION      63 

pyogenic  meningitis  and  in  cerebrospinal  meningitis,  but  in  the 
acute  stages  of  tuberculous  meningitis  and  in  poliomyelitis  it  is 
demonstrable.  In  diabetes  mellitus,  as  a  rule,  this  substance  is 
decidedly  increased,  usually  in  close  relation  to  the  degree  of 
glycosuria. 

The  potassium  content  of  the  cerebrospinal  fluid  obtained  be- 
fore death  is  in  general  higher  in  acute  than  in  chronic  lesions  of 
the  cerebrospinal  system,  but  no  relation  exists  between  the  potas- 
sium content  and  the  cellular  richness  and  globulin  reaction  of  this 
fluid  (Rosenbloom;  Andrews). 

Cytodiagnosis  is  of  some  value  in  differentiating  certain  acute  and 
chronic  types  of  meningeal  disease.  Thus,  when  the  clinical  picture 
suggests  acute  meningitis,  a  lymphocytosis  implies  tuberculosis  as 
the  factor,  rather  than  the  meningococcus,  pneumococcus,  streptococ- 
cus, staphylococcus,  or  other  bacteria,  in  all  of  which  a  polynucleosis 
is  the  rule.  Meningitides  of  long  standing  and  those  nearing  recovery 
cannot,  however,  be  judged  by  this  criterion,  for  in  such  instances 
there  is  ordinarily  a  definite  lymphocytosis.  In  cerebrospinal 
syphilis,  tabes,  paresis,  uremia,  and  other  lesions  that  excite  infiltra- 
tion of  the  meninges  a  lymphocytosis  is  also  to  be  expected.  In  view 
of  the  foregoing  facts  it  is  obvious  that  cytodiagnosis  of  the  cerebro- 
spinal fluid  can  be  relied  on  only  when  interpreted  in  relation  with 
all  the  other  clinical  findings  of  the  case  in  question.  The  detection 
of  cancer-cells  in  the  cerebrospinal  fluid  has  led  to  the  antemortem 
diagnosis  of  carcinoma  of  the  central  nervous  system  (Widal).  The 
presence  of  many  erythrocytes  and  lymphocytes  in  a  yellowish 
fluid  of  high  coagulability  is  a  syndrome  suggestive  both  of  dural 
sarcoma  and  of  meningomyelitis. 

Bacteriologic  examination  of  the  cerebrospinal  fluid  includes  the 
microscopic  study  of  stained  cover-glass  films  prepared  from  the 
centrifugalized  sediment,  supplemented,  in  appropriate  cases,  by 
suitable  cultural  methods.  Thus  one  can  differentiate  with  absolute 
surety  true  meningococcus  cerebrospinal  fever  from  meningitides 
due  to  the  streptococcus,  staphylococcus,  pneumococcus,  tubercle 
bacillus,  and  other  bacteria.  The  offending  bacterium  can  usually 
be  identified  by  direct  examination  of  the  stained  specimen,  animal 
inoculation  being  called  for  only  exceptionally.  Even  in  tuberculous 
meningitis,  contrary  to  current  belief,  the  tubercle  bacillus  is  found 
in  from  75  to  90  per  cent,  of  all  cases,  if  the  spreads  be  made  fron 
the  delicate  coagulum  of  the  fluid  (G.  Canby  Robinson).  In  pneu- 
monia Rohdenburg  reports  a  high  percentage  (87  per  cent.)  oi 
positive  cultures  in  fatal  cases,  with  a  fair  proportion  (34  per  cent.) 


64  PHYSICAL   DIAGNOSIS 

in  those  recovering.  In  trypanosomiasis  the  Trypanosome  gam- 
biense  persists  in  the  spinal  fluid  long  after  it  has  been  driven  from 
the  blood  and  the  glands  by  the  use  of  atoxyl. 

The  presence  of  a  positive  Wassermann  reaction  in  the  cerebro- 
spinal  fluid  is  of  great  value  in  the  diagnosis  of  syphilis  of  the 
central  nervous  system,  and  in  paresis  and  tabes  a  positive  colloidal 
gold  test  is  helpful. 

Visceral  Paracentesis. — Exploratory  puncture  of  the  spleen  has 
become  a  routine  clinical  measure  among  those  who  deal  with  trop- 
ical splenomegaly  and  with  obscure  malarial  infections,  and  the  pro- 
cedure is  also  of  great  utility  in  certain  cases  of  abscess  and  of  hyda- 
tid  disease.  In  enteric  fever  splenic  puncture  is  scarcely  justifiable, 
in  view  of  the  adequacy  of  other  less  perilous  methods  of  diagnosis. 
Hemophilia  and  active  congestion  of  the  organ  forbid  splenic  punc- 
ture. Using  a  very  delicate  hollow  needle  (not  larger  than  56  gage), 
the  spleen  is  pierced  either  through  the  tenth  left  intercostal  space 
in  the  midaxillary  line,  or,  if  it  be  greatly  enlarged,  at  a  convenient 
point  below  the  left  costal  margin.  During  the  operation,  which 
must  be  done  quickly,  the  patient  should  hold  his  breath,  so  as  to 
minimize  the  risk  of  tearing,  with  the  point  of  the  needle,  the  par- 
enchyma of  the  organ  or  its  capsule.  These  possible  accidents, 
which  may  be  followed  by  hemorrhage,  peritonitis,  and  even  splenic 
rupture,  are  more  prone  to  occur  when  the  spleen  is  soft  and  friable, 
as  in  enteric  fever,  than  when  it  is  hard  and  compact,  as  in  ague  cake. 

Puncture  of  the  liver  is  generally  made  under  general  anesthesia, 
the  organ  being  entered  by  a  very  fine  needle  passed  through  a  right 
lateral  or  posterior  interspace,  well  below  the  upper  level  of  hepatic 
flatness,  i.  e.,  the  seventh  or  eighth  interspace  in  the  right  axillary 
space.  Hepatic  puncture  has  settled  the  diagnosis  in  many  a  case 
of  pyogenic  or  amebic  abscess,  and  of  echinococcus  infection  of  the 
liver;  it  should  not  be  attempted  in  acute  yellow  atrophy,  nor  under 
the  circumstances  noted  above  as  contraindications  to  puncture  of 
the  spleen. 

Puncture  of  the  kidney  is  attempted  only  when  a  large  renal  swell- 
ing can  be  made  out  just  beneath  the  abdominal  wall,  exploratory 
laparotomy  being  a  more  satisfactory  means  of  inquiry  in  most 
instances. 

Puncture  of  the  lung  is  occasionally  helpful  in  detecting  and  in 
orienting  pulmonary  and  bronchiectatic  cavities,  and  in  obtaining 
therefrom  secretion  for  laboratory  examination.  For  this  purpose 
a  long,  fine  needle  and  aspiration  syringe  should  be  used,  the  puncture 
being  made  where  the  surface  signs  suggest  an  excavation,  the  subject 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       65 

meanwhile  controlling  thoracic  movement.  If  the  needle-point, 
after  penetration  of  the  lung,  can  be  freely  swept  through  a  consider- 
able arc,  a  large  cavity  is  suggested,  though  a  surer  guide  is  the  aspir- 
ation of  a  large  amount  of  offensive  secretion;  if,  however,  the  patient 
has  freely  expectorated  just  before  the  paracentesis  is  made,  a  cavity 
may  yield  no  fluid  whatever.  A  bronchial  or  pulmonary  cavity, 
rather  than  empyerna,  is  indicated  by  the  aspiration,  from  a  compara- 
tively deep  level,  of  a  mixture  of  air  and  mucopus  containing  elastic 
fibers  and  other  microscopic  evidences  of  tissue  disintegration. 

FLUOROSCOPY  AND  RADIOGRAPHY 

Examination  by  means  of  the  Rontgen  ray,  though  more  often 
corroborative  of  other  findings  than  primarily  diagnostic,  has  a  dis- 
tinct place  in  physical  diagnosis  which  no  student  of  this  subject 
can  afford  to  ignore.  The  average  internist  cannot  hope,  nor  does 
he  desire,  to  have  more  than  a  bowing  acquaintance  with  #-ray  tech- 
nic,  but  it  is  highly  desirable  that  his  familiarity  with  radioscopic 
shadows  and  radiographs  should  be  sufficiently  thorough  to  permit 
intelligent  association  of  his  clinical  impressions  with  the  views  of 
the  trained  specialist  in  ^-ray  work. 

Technic. — Detailed  consideration  of  x-ray  technic  and  of  the  risks 
inseparable  therefrom  is  not  germane  to  the  plan  of  this  book,  and 
for  this  information  treatises  dealing  with  this  highly  specialized 
subject  should  be  consulted.  It  may,  however,  be  stated  that  the 
equipment  required  for  this  work  includes  some  source  of  electric 
current,  derived  from  an  ordinary  incandescent-light  service,  from  a 
storage  battery,  or  from  a  static  machine;  a  coil  capable  of  converting 
this  current  into  one  of  greatly  increased  power  (save  when  the 
electric  supply  is  generated  by  a  static  machine) ;  and  an  x-ray  tube, 
consisting  of  a  glass  vacuum  bulb  inclosing  a  positive  and  a  negative 
pole,  made  of  platinum  and  wired  to  the  current  generator.  The 
current,  passing  through  the  tube,  jumps  the  vacuum  gap  from  the 
positive  to  the  negative  pole,  and  produces  luminous  rays  having  the 
property  of  penetrating  ordinarily  opaque  substances  and  of  creating 
shadows  visible  with  the  aid  of  a  fluoroscope,  and  permanently  record- 
able upon  a  sensitized  photographic  plate. 

Fluoroscopy. — The  fluoroscope,  devised  for  the  direct  inspection 
of  the  shadows  during  rontgenization,  consists  of  a  pyramidal  hood 
with  an  apex  provided  with  an  opening  for  the  observer's  eyes  and 
a  base  made  of  a  fluorescent  screen  which  becomes  luminous  when 
acted  upon  by  x-rays.  With  the  area  to  be  examined  interposed 

5 


66  PHYSICAL   DIAGNOSIS 

between  the  x-ra.y  tube  and  the  fluoroscope  the  shadows  cast  by  dense 
substances  within  the  body  cavities  and  other  parts  are  clearly  visible 
upon  the  surface  of  the  luminous  screen.  The  examinations  should, 
of  course,  be  conducted  in  a  dark-room,  in  which  the  examiner 
ought  to  remain  long  enough  to  acquire  a  keen  perception  of  faint 
shadows,  before  attempting  to  judge  them  with  the  fluoroscope. 

Radiography. — Except  when  effusions  are  being  investigated,  in 
which  event  the  upright  position  is  preferable,  radiographs  of  the 
chest  and  abdomen  are  made  with  the  subject  in  recumbency,  the 
body  being  turned  so  as  to  bring  the  lesion  to  be  photographed 
directly  over  a  sensitized  plate  placed  beneath  the  adjacent  parietal 
parts.  In  thoracic  work  the  scapulae  are  to  be  swept  outward  by  the 
patient  clasping  the  hands  over  the  head,  and  the  subject  cautioned 
to  make  as  little  respiratory  movement  as  possible.  The  correct 
posture  having  been  assumed,  the  .r-ray  tube  is  adjusted  and  the 
exposure  made,  the  resulting  negative  and  print  therefrom  being 
carefully  examined,  in  the  light  of  the  other  clinical  findings,  and 
with  the  aid  of  a  skilled  radiographer's  opinion. 

Applied  to  internal  medicine,  the  Rontgen-ray  is  helpful  chiefly 
in  the  examination  of  the  thoracic  organs,  and  in  some  instances 
lesions  of  the  heart  and  great  vessels,  bronchopulmonary  system, 
and  mediastinum  are  revealed  only  by  this  means.  In  such  exami- 
nations fluoroscopy  is  superior  to  radiography,  for  it  is  a  compara- 
tively simple  procedure  to  inspect  the  chest  contents  with  a  fluoro- 
scope, while  a  photographic  negative  takes  longer  to  make,  and,  unless 
instantaneously  exposed,  is  blurred  by  the  cardiac  and  respiratory 
movements.  In  abdominal  work,  on  the  other  hand,  radiography 
usually  gives  more  accurate  data  than  the  fluoroscope,  but  neither 
is  dependable  unless  the  gastro-intestinal  tract  is  practically  empty 
at  the  time  of  the  examination.  Recently  great  advances  have  been 
made  in  the  differentiation  of  gastric  and  duodenal  lesions  by  the 
study  of  serial  radiographs  made  at  fixed  intervals  after  the  pa- 
tient's ingestion  of  a  draft  of  bismuth-buttermilk.  The  Cray's 
field  of  usefulness  in  abdominal  diagnosis  also  includes  the  detection 
of  calculi,  especially  of  the  kidney  and  of  the  urinary  bladder,  and, 
with  less  certainty,  of  the  gall-bladder  and  ducts.  The  shape  and 
size  of  the  abdominal  organs,  as  well  as  the  presence  of  new 
growths  that  may  invade  them  and  other  intra-abdominal  struc- 
tures, are  also  demonstrable  by  the  x-ray. 

The  normal  and  pathologic  #-ray  pictures  of  the  thoracic  and 
abdominal  organs,  and  their  application  to  the  diagnosis  of  special 
lesions,  are  referred  to  later,  in  connection  with  other  physical  signs. 


METHODS   AND    TECHNIC    OF   PHYSICAL   EXAMINATION      67 

THE  TUBERCULIN  REACTION 

Here  may  be  mentioned  the  several  types  of  the  tuberculin  reaction 
observed  in  different  forms  of  tuberculosis,  and,  properly  employed, 
capable  of  serving  as  valuable,  sometimes  indispensable,  clues  in 
the  diagnosis  of  obscure  cases. 

Koch's  tuberculin  test  consists  of  the  hypodermic  injection  of  a 
definite  quantity  of  tuberculin,  whereby  moderate  fever  and  other 
systemic  disturbances  are  produced  in  a  tuberculous  subject,  whereas 
in  a  healthy  person  no  appreciable  symptoms  arise.  Ordinarily, 
this  test  is  resorted  to  only  after  all  other  methods  of  diagnosis  have 
failed,  for  there  is  always  a  possibility,  remote  though  it  be,  that  the 
injection  of  tuberculin,  by  profoundly  depressing  the  body's  resistance, 
may  light  up  latent  tuberculous  foci.  Koch's  old  tuberculin  (T.  O.) 
is  generally  used  for  diagnostic  purposes,  the  conservative  initial 
dose  being  0.2  mg.,  which,  if  insufficient  to  cause  a  reaction, 
should  be  followed,  at  intervals  of  a  few  days,  by  successive  doses 
of  1,3,  and  5  mg.,  until  a  reaction  occurs.  Experience  has  shown 
that  if  this  routine  be  followed  by  negative  results,  no  reaction  will 
occur  with  the  higher  dosage  (10  mg.)  advocated  by  some  investi- 
gators. A  positive  reaction  occurring  after  a  second  or  a  third 
injection  has  not  the  same  clinical  value  as  a  primary  positive 
finding,  for  the  first  injection  may,  by  a  sensitizing  process,  cause 
a  non-tuberculous  subject  to  react. 

The  criterion  of  a  positive  tuberculin  reaction  is  fever,  which  should 
amount  to  at  least  i£°  F.  within  from  ten  to  twenty-four  hours  after 
the  injection;  such  by-effects  as  rigors,  aching,  nausea,  vomiting, 
and  hemoptysis,  while  suggestive,  do  not  constitute,  in  the  absence 
of  a  rise  of  temperature,  a  positive  reaction.  As  a  rule,  the  subject's 
fever  and  indisposition  disappear  within  from  twenty-four  to  thirty- 
six  hours  after  their  onset. 

The  cutaneous  tuberculin  test  of  von  Pirquet  relates  to  an 
afebrile  local  reaction  produced  in  the  tuberculous  subject  by  inocu- 
lation of  the  skin  with  tuberculin,  after  the  manner  employed  in  cow- 
pox  vaccination.  The  "vaccine"  consists  of  Koch's  old  tuberculin, 
diluted  with  i  part  of  a  5  per  cent,  solution  of  carbolic  acid  in  glycerin 
and  2  parts  of  normal  saline  solution.  Two  drops  of  this  mixture 
are  placed  on  the  skin  of  the  arm,  about  2  inches  (5  cm.)  apart,  and 
through  each  drop  an  abrasion  is  made  by  means  of  a  sterile  needle. 
A  control  inoculation  is  then  made  in  the  neighborhood  with  normal 
saline  solution.  If  the  reaction  be  positive,  the  site  of  inoculation 
will  show,  within  twenty-four  or  forty-eight  hours,  an  areolated 


68  PHYSICAL    DIAGNOSIS 

papule  about  one-half  inch  (1.25  cm.)  in  diameter,  and  of  a  bright 
red  color,  which  later  deepens,  and,  fading  during  the  course  of  a 
few  days,  sometimes  leaves  a  pigmented  area  at  its  site.  Rarely, 
turbid  vesicles  appear,  and  occasionally  a  small  urticaria!  patch 
springs  up  at  the  point  of  inoculation.  The  control  inoculation,  of 
course,  shows  none  of  the  changes  just  noted. 

Von  Pirquet's  test  is  of  little  practical  value  in  diagnosing  tuber- 
culosis in  the  adult,  since  positive  reactions  are  not  unusual  in 
those  who  have  passed  the  age  of  puberty,  despite  the  fact  that  the 
subject  is  symptomatically  free  from  all  tuberculous  taint.  This  is 
as  one  would  expect,  since  few  of  us  reach  this  period  of  life  without 
having  been  at  some  time  infected  with  Koch's  bacillus.  In  children 
the  test  is  more  useful,  and  its  value  increases  in  direct  relation  with 
the  youth  of  the  child.  From  these  remarks  it  is  obvious  that  the 
cutaneous  reaction  is  a  delicate  indicator  of  latent  tuberculosis,  in 
which,  it  must  be  added,  positive  results  are  obtained  much  more 
constantly  than  in  active  lesions. 

Calmette's  ophthalmoreaction  is  the  specific  conjunctivitis 
excited  by  the  instillation  of  a  weak  solution  of  tuberculin  in  the  eye 
of  a  tuberculous  subject,  no  such  reaction  being  produced  by  this 
test  in  a  person  free  from  tuberculous  taint.  One  minim  of  a  0.5 
per  cent,  glycerin-free  solution  of  dry  tuberculin1  is  dropped  into 
the  inner  canthus  of  the  eye,  whereupon,  if  the  subject  be  tuberculous, 
acute  congestion  of  the  conjunctiva,  with  redness  and  swelling  of 
the  lacrimal  caruncle,  develops,  usually  within  from  three  to  six 
hours  after  the  instillation,  and,  finally,  in  intense  reactions,  the 
conjunctival  surfaces  become  bathed  with  a  profuse  puriform  exu- 
date  within  the  next  six  hours  or  so.  In  the  exceptional  instance  both 
eyes  are  inflamed  (S.  H.  Long).  The  inflammation  thus  produced 
generally  abates  within  twenty-four  or  thirty-six  hours,  and  entirely 
disappears  by  the  end  of  three  or  four  days.  It  is  attended  by  free 
lacrimation  and  by  a  sensation  of  moderate  heat  and  burning  in  the 
instilled  eye.  The  ophthalmoreaction  is  contraindicated  by  any  sort 
of  ocular  lesion  whereby  the  integrity  of  the  eye  is  impaired,  nor  is 
it  to  be  employed  when  there  is  reason  to  suspect  a  very  active  form 
of  tuberculosis,  for  here  the  unduly  low  conjunctival  resistance  plus 
the  irritant  effect  of  the  tuberculin  might  lead  to  serious  local  damage. 
The  aggravation  of  a  preexisting  ocular  lesion  by  the  instillation  of 

1  The  test  solution  is  marketed  in  glass  capsules,  and  also  in  the  form  of 
discs,  one  of  which,  dissolved  in  i  c.c.  of  sterile  water,  makes  a  i  per  cent 
solution.  For  fear  of  exciting  too  violent  a  reaction  it  is  better  to  use  a  tuber- 
culin solution  of  one-half  this  strength. 


METHODS    AND    TECHNIC    OF    PHYSICAL    EXAMINATION       69 

tuberculin  may  result  in  violent  conjunctivitis,  iritis,  corneal 
ulceration,  or  pannus. 

The  intensity  of  the  reaction  has  no  fixed  relation  to  the  severity 
of  the  tuberculous  infection:  incipient  and  mild  cases  rarely  fail  to 
react,  while  only  about  50  per  cent,  of  severe  infections  are  positive. 
A  positive  reaction  obtained  at  a  second  test,  in  the  eye  unaffected 
by  the  primary  instillation,  is  of  no  clinical  value  whatever,  for  under 
such  circumstances  the  development  of  conjunctivitis  indicates 
merely  the  local  sensitizing  action  of  the  earlier  instillation,  whereby 
the  conjunctiva  may  react  to  tuberculin,  even  if  the  subject  be  per- 
fectly healthy.  Conjunctival  congestion,  it  is  interesting  to  note, 
is  lighted  up  by  the  subcutaneous  injection  of  tuberculin  in  a  patient 
having  recently  reacted  to  the  ophthalmic  test. 

Mora's  reaction  consists  of  the  eruption  of  pale  or  of  red  papules 
over  a  cutaneous  area  after  the  application  thereto  of  an  ointment 
made  of  5  c.c.  of  old  tuberculin  and  5  gm.  of  anhydrous  wool-fat. 
A  reaction  of  this  sort  has  virtually  the  same  significance  as  a  posi- 
tive von  Pirquet's  test. 


SECTION   II 
EXAMINATION  OF  THE  THORAX 


CLINICAL  ANATOMY 

THE  thorax  consists  of  a  bony  framework  formed  by  the  sternum, 
the  ribs,  the  vertebrae,  and  their  cartilages,  invested  by  a  musculature 
of  varying  density;  it  incloses  the  esophagus,  trachea,  bronchi,  lungs, 
heart,  and  great  vascular  trunks,  and  surrounds  at  its  base  the  import- 
ant viscera  of  the  upper  part  of  the  abdominal  cavity.  The  bony 
thorax  is  shaped  like  a  truncated  cone,  whose  superior  aperture  is 
formed  by  the  upper  border  of  the  ster- 
num, the  first  ribs,  and  the  first  thoracic 
vertebra,  the  inferior  aperture  being  floored 
by  the  diaphragm.  A  cross-section  of 
the  normal  adult  thorax  is  elliptical  (Fig. 
20),  the  transverse  axis  being  decidedly 
longer  than  the  anteroposterior;  in  the 

young  child,  however,  the  two  axes  are 
Fig.  so. — Transverse  section  „  ,  ,     ,,  •  i         .1 

of  a  normal  adult  thorax.       practically   equal,    and    this   is    also    the 

case  in  certain  types  of  chest  deformities 

resulting  from  pathologic  processes.      (See    Pathologic    Types    of 
Thorax,  p.  77.) 

The  average  vertical  measurement  of  the  normal  chest  is  13  inches 
(32.5  cm.)  in  men,  and  n.8  inches  (29.5  cm.)  in  women,  the  antero- 
posterior diameters  being  7.7  and  7  inches  (19.2  and  17.5  cm.), 
and  the  transverse  diameters  10.5  and  9.8  inches  (26.2  and  24.5  cm.) 
for  the  respective  sexes  (Bessenen).  Fourmentin's  "thoracic  index" 
(anteroposterior  diameter  x  100  -=-  transverse  diameter)  equals, 
in  the  normal  man,  72  (Woods  Hutchinson).  The  normal  chest 
expansion  varies  from  i£  to  4  or  5  inches  (3.8  to  10  or  12.5  cm.), 
while  the  circumference,  according  to  Otis's  measurements,  averages 
34  inches  (85  cm.)  in  men  and  29.5  inches  (73.7  cm.)  in  women. 
The  respiratory  capacity  of  the  average  male  thorax  is  approximately 
3.3  liters  (201  cubic  inches),  or  about  20  c.c.  for  each  centimeter  of 
stature. 
70 


EXAMINATION    OF    THE    THORAX  71 

A  perfectly  symmetric  chest  is  rare,  although  conspicuous  devia- 
tions from  the  normal  contour  are  seldom  met  with,  except  in  those 
who  have  acquired  local  muscular  overdevelopment,  usually  as  the 
result  of  their  occupation  or  a  similar  cause.  The  one-sided 
chest  fulness  of  the  blacksmith  and  of  the  iron  puddler  and  the 
drooping  shoulder  of  the  hod-carrier  are  familiar  types  of  this  sort 
of  asymmetry.  Aside  from  such  influences,  however,  the  right  half 
of  the  chest  is  generally  somewhat  larger  than  the  left  half  in  right- 
handed  persons,  and  there  are  few  adults,  even  in  perfect  health, 
that  do  not  show  a  moderate  dextral  inclination  of  the  dorsal  spine. 
In  those  who  are  left-handed  the  asymmetry  is,  of  course,  left  sided. 

NORMAL  LANDMARKS 

Study  of  the  thoracic  organs  is  facilitated  by  the  use  of  the  normal 
landmarks,  bony  and  muscular,  upon  the  walls  of  the  chest,  as  well 
as  by  the  aid  of  a  number  of  arbitrary  lines  drawn  upon  its  surface. 
Having  detected  a  given  sign,  it  is  first  oriented  in  a  certain  area  of 
the  thorax,  and  then  more  accurately  localized  by  determining  its 
precise  relation  to  one  of  these  fixed  anatomic  landmarks  and  to  a 
surface  line.  For  example:  "A  systolic  pulsation  in  the  fifth  left 
intercostal  space,  one-half  inch  to  the  right  of  the  left  midclavicular 
line,"  technically  describes  the  situation  of  the  normal  apex-beat  of 
the  heart. 

The  clavicles  are  conspicuous  landmarks  upon  the  anterior  chest- 
wall:  a  moderate  prominence  of  these  bones  is  not  incompatible 
with  good  health,  and  even  bilateral  deepening  of  the  fossae  above 
and  below  the  collar-bones  may  exist,  without  the  slightest  implication 
of  the  pulmonary  apices.  Unilateral  depression  in  one  of  these  regions, 
on  the  contrary,  is  extremely  significant  of  an  apical  lesion,  especially 
if  the  sunken  area  expands  laggingly  and  imperfectly  during  respira- 
tion. The  sternal  ends  of  the  clavicles  correspond  to  the  level  of  the 
disc  between  the  second  and  third  thoracic  vertebrae.  The  depressed 
area  below  the  junction  of  the  middle  and  outer  thirds  of  the 
clavicle,  between  the  pectoralis  major  and  the  deltoid  muscles,  is 
known  as  Mohrenheim's  fossa  (Fig.  21). 

Lloyd  Jones  has  noted  that  in  right-handed  adults  the  right  clavicle 
is  tilted  more  than  the  left,  that  in  the  left-handed  the  left  clavicle 
is  tilted  more  than  the  right,  and  that  in  the  ambidextrous  the  clavicles 
slope  equally. 

The  sternum,  bounded  above  by  the  suprasternal  notch  and 
below  by  the  ''pit  of  the  stomach"  (scrobiculus  cordis),  is  the  seat 
of  two  important  surface-markings:  the  angle  of  Louis  (angulus 
Ludovici)  and  the  xiphisternal  joint  (Fig.  21).  The  angle  of  Louis 


72  PHYSICAL   DIAGNOSIS 

is  a  transverse  ridge,  always  palpable  and  usually  visible,  formed 
by  the  articular  surfaces  of  the  manubrium  and  the  gladiolus,  and 
corresponding  in  front  to  the  level  of  the  second  costal  cartilage,  and 
behind  to  the  third  thoracic  vertebra.  Since  this  prominence  indicates 
the  position  of  the  second  rib,  it  serves  as  an  accurate  landmark  in 
counting  the  ribs.  The  xiphisternal  articulation  (Fig.  21)  is  situated 
just  below  the  sternal  end  of  the  seventh  costal  cartilages  and  cor- 
responds to  the  disc  between  the  ninth  and  tenth  thoracic  vertebrae. 


'Suprasternal  notch 

*am  ^ 

Supraclavicuh'.r  fossa- 


Infraclavicular 
(Mohrenheim's)  fossa 


Angle  of  Louis 


—  Subcostal  (epigastric) 
Sibson's  furrow —  angle 

"tScrobiculus  cordis 


Base  of  costal  arch 


Fig.  2 1 . — Normal  thoracic  landmarks 

The  ribs  and  intercostal  spaces  are  usually  taken  as  the  horizontal 
topographic  lines,  the  number  of  an  interspace  being  that  of  the  rib 
immediately  above  it.  Owing  to  the  obliquity  of  the  ribs,  their 
sternal  ends  are  at  a  lower  level  than  their  vertebral :  the  first  rib  in 
front  is  in  the  plane  of  the  fourth  rib  behind,  and  the  anterior  level 
of  each  of  the  next  five  ribs  (second  to  seventh,  inclusive)  corresponds 
to  the  posterior  level  of  the  fourth  rib  below  it.  The  first  seven  (true) 
ribs  articulate  individually  with  the  sternum,  but  the  lower  five  (false) 
lack  this  direct  attachment  to  the  breast-bone.  In  the  well-developed 
adult  the  ribs  are  visible  only  upon  the  lateral  walls  of  the  lower 


EXAMINATION    OF    THE    THORAX  73 

chest.  The  upper  ribs  run  horizontally  outward  from  their  sternal 
attachments,  but  as  the  epigastrium  is  approached  their  obliquity 
increases,  so  that  the  epigastric  or  subcostal  angle,  formed  by  the 
substernal  divergence  of  the  costal  margins,  is  approximately  an 
angle  of  70°  (Fig.  21).  With  inspiration  the  subcostal  angle  is 
more  obtuse  than  with  expiration,  owing  to  the  exaggerated  obliquity 
of  the  ribs  during  the  latter  period  of  breathing. 

In  counting  the  ribs  on  the  anterior  chest-wall  Louis'  angle  and  the 
lower  border  of  the  pectoralis  major  muscle  (Sibson's  furrow)  are 
accurate  indices  to  the  second  and  the  fifth  ribs,  respectively.  It  is 
much  easier  to  find  the  first  rib  by  counting  upward  from  the  former 
landmark  than  by  direct  palpation  backward  and  downward  under 
the  clavicle.  The  lowest  part  of  the  costal  arch  corresponds  to  the 
cartilage  of  the  tenth  rib.  Laterally,  the  highest  visible  slip  of  the 
serratus  magnus  muscle  is  a  guide  to  the  fifth  rib.  Posteriorly,  the 
scapula  extends  from  the  second  to  the  seventh  rib  inclusive,  the 
inner  end  of  its  spine  being  at  the  level  of  the  third  thoracic  spine 
and  its  inferior  angle  corresponding  to  the  seventh  thoracic  ver- 
tebra. The  scapulae  do  not  stand  out  prominently  from  the  normal 
thorax,  but  lie  snugly  against  it.  The  "scaphoid  scapula" 
(Graves),  with  concave  vertebral  borders,  is  generally  considered 
a  normal  variation  and  not  a  developmental  anomaly,  as  formerly 
believed.  Other  bony  landmarks  useful  in  counting  the  ribs 
in  the  back  are  the  seventh  cervical  vertebral  spine  (vertebra 
prominent),  directly  below  which  is  the  joint  of  the  first  thoracic 
vertebra  and  the  first  rib.  The  free  tips  of  the  eleventh  and 
twelfth  (floating)  ribs  correspond  to  the  spines  of  the  eleventh 
and  twelfth  thoracic  vertebrae,  and  are  palpable  outside  the 
erector  spinae  muscles.  Each  thoracic  spine  from  the  second  to 
the  ninth  inclusive  corresponds  in  number  to  that  of  the  rib  next 
below  it  serially  ;  the  tenth  spinous  process  is  opposite  the  tenth 
interspace. 

The  upper  intercostal  spaces,  of  which  the  second  usually  is  the 
widest,  are  readily  palpable,  especially  in  front,  but  it  is  sometimes 
a  difficult  matter  to  feel  the  lower  interspaces,  owing  to  their  narrow- 
ness. 

The  nipple  in  a  man  usually  lies  between  the  fourth  and  the  fifth 
ribs,  about  4  inches  (10  cm.)  from  the  center  of  the  sternum.  A 
woman's  nipple  is  situated  somewhat  below  the  center  of  the  mam- 
mary gland,  which  covers  the  chest-wall  from  the  second  to  the  sixth 
or  seventh  ribs,  and  from  the  sternal  border  to  the  anterior  limit 
of  the  axilla.  The  female  nipple  is  not  a  reliable  surface-marking, 
owing  to  the  variable  size  and  shape  of  a  woman's  breast. 


74  PHYSICAL   DIAGNOSIS 

TOPOGRAPHIC  LINES  AND  AREAS 

In  connection  with  the  foregoing  anatomic  landmarks  the  clinician 
makes  use  of  a  number  of  imaginary  vertical  lines,  drawn  parallel 
to  the  long  axis  of  the  torso,  these  lines,  in  their  order  from  sternum 
to  spine,  being  as  follows: 

The  midsternal  (anterior  median)  line,  passing  through  the 
middle  of  the  sternum,  from  the  cricoid  cartilage  above  to  the  tip 
of  the  xiphoid  appendix  below.  Prolonged  downward,  this  line 
divides  the  abdomen  laterally  and  ends  in  the  middle  of  the  symphysis 
pubis. 

The  sternal  (lateral  sternal)  line,  paralleling  the  lateral  border  of 
the  sternum,  and  continuous  below  with  the  line  of  the  costal  arch. 

The  parasternal  line,  drawn  midway  between  the  sternal  line  and 

The  midclavicidar  (mammillary,  nipple)  line,  let  fall  from  the 
middle  of  the  clavicle.  Projected  downward  this  line  crosses  the 
costal  arch  at  the  level  of  the  ninth  costal  cartilage,  and  is  continuous 
with  the  vertical  Poupart  line,  which  terminates  in  the  middle  of 
Poupart's  ligament.  This  line,  although  commonly  termed  "mam- 
millary," rarely  passes  through  the  nipple,  frequently  running  wide 
of  this  point  in  the  male,  and  almost  invariably  doing  so  in  the  female. 

The  anterior  axillary  line,  running  downward  from  the  anterior 
fold  of  the  axilla. 

The  midaxttlary  line,  drawn  from  the  middle  or  apex  of  the 
axilla. 

The  posterior  axillary  line,  dropped  from  the  posterior  fold  cf  the 
axilla. 

The  scapular  line,  falling  perpendicularly  through  the  inferior 
angle  of  the  scapula. 

The  midspinal  (posterior  median)  line,  corresponding  to  the 
middle  of  the  spinal  column. 

For  an  ordinary  clinical  examination  the  ribs  and  interspaces  are 
sufficiently  definite  horizontal  landmarks,  although  in  certain  instances 
it  may  be  advisable,  for  the  sake  of  technical  description,  to  localize 
a  physical  sign  with  relation  to  certain  imaginary  horizontal  lines. 
Drawn  across  the  long  axis  of  the  trunk,  these  lines  may  be  indicated: 

The  cricoclavicular  line,  drawn  from  the  cricoid  cartilage  of  the 
larynx  to  the  point  upon  the  clavicle  crossed  by  the  upward  projection 
of  the  anterior  axillary  line. 

The  clavicular  line,  following  the  course  of  the  clavicles. 

The  third  costal  line,  drawn  from  the  third  chondrosternal 
articulation  to  the  anterior  axillary  line. 


yajt&b**&f  \X\\\\\ 

A  \  ~\    V  ;//V\\' 


«*     C? 

I 


UYC 

H  >sr°^?sQC1 


Axillary 


75 


PHYSICAL   DIAGNOSIS 


The   sixth    costal    line,  drawn    from    the    sixth    chondrosternal 
articulation  to  the  posterior  axillary  line. 


The  line  of  the  costal  arch,  continuous  with  the  sternal  line  and 
following  the  costal  margin. 

The  infracostal  line,  connecting  the  lower  borders  of  the  tenth 
costal  cartilages. 


EXAMINATION    OF    THE    THORAX  77 

The  scapular  spinal  line,  corresponding  to  the  spines  of  the 
scapulae. 

The  infrascapular  line,  at  the  level  of  the  inferior  angles  of  the 
scapulae. 

The  line  of  the  twelfth  thoracic  vertebra,  curving  outward  and 
downward  from  the  spinous  process  of  this  bone  to  the  posterior 
axillary  line. 

The  following  topographic  regions  (Fig.  23)  may  be  mapped  out 
upon  the  surface  of  the  chest  by  the  use  of  the  foregoing  lines: 

The  sternal  region,  corresponding  to  the  sternum,  extending  verti- 
cally from  the  suprasternal  notch  to  the  tip  of  the  xiphoid  process, 
and  horizontally  between  the  sternal  lines. 

The  supraclavicular  region,  or  the  triangular  space  over  and  above 
the  clavicles,  bounded  externally  by  the  cricoclavicular  lines. 

The  infraclavicular  region,  bounded  above  by  the  clavicle,  below 
by  the  third  costal  line,  externally  by  the  anterior  axillary  line,  and 
internally  by  the  sternal  line. 

The  mammary  region,  lying  between  the  third  and  sixth  costal, 
and  the  anterior  axillary  and  sternal,  lines. 

The  hypochondriac  or  inframammary  region,  lying  below  the  sixth 
costal  line,  being  limited  internally  and  below  by  the  line  of  the 
costal  margin,  and  externally  by  the  anterior  axillary  line. 

The  axillary  region,  extending  from  the  apex  of  the  axilla  to  the 
sixth  costal  line. 

The  infra-axillary  region,  from  the  sixth  costal  line  to  the  costal 
margin,  the  lateral  boundaries  of  both  axillary  areas  being  the 
anterior  and  posterior  axillary  lines. 

The  suprascapular  and  the  scapular  regions  overlie  the  supra- 
spinous  and  the  infraspinous  fossae  of  the  scapula  respectively;  the 
interscapular  region  includes  that  part  of  the  back  between  the 
scapulas;  and  the  infrascapular  region  extends,  between  the  right 
and  left  posterior  axillary  lines,  from  the  inferior  scapular  line  to  that 
of  the  twelfth  thoracic  vertebra. 

PATHOLOGIC  TYPES  OF  THORAX 

Of  the  several  types  of  bilateral  abnormalities  of  the  thorax,  some 
are  so  constantly  associated  with  definite  diseases  as  to  serve  as 
almost  certain  clues  to  these  conditions,  while  others  betray  simply 
retarded  or  erratic  physical  development.  The  first  group  includes 
the  forms  of  chest  peculiar  to  phthisis,  to  hypertrophic  emphysema, 
to  rickets,  and  to  syringomyelia;  the  second  group  comprises  those 


PHYSICAL   DIAGNOSIS 


observed  in  the  thin,  undeveloped  individual  and  in  the  woman  that 
laces  too  tightly. 

The  Phthisical  Thorax  (Pterygoid;  Paralytic;  Alar).— The 
typical  chest  of  the  phthisical  subject  appears  long,  emaciated, 
deficient  in  expansion,  and  often  shows  circumscribed  areas  of  flatness 
and  of  retraction  (Figs.  24  and  25).  The  common  belief,  current 
since  the  days  of  Galen,  that  the  phthisical  thorax  is  shallow  and 
flat,  is  true  of  some  cases,  but  in  others,  especially  in  those  with  lesions 
far  advanced,  the  anteroposterior  diameter  is  greater  than  normal 

and  the  transverse  outline 
of  the  chest  deep  and 
round  (Woods  Hutchinson) 
(Fig.  26). 

The  neck  is  likely  to  be 
long  and  slender,  the  larynx 
conspicuous,  the  clavicles 
prominent,  and  the  supra- 
clavicular  and  infraclavic- 
ular  areas  abnormally  and 
unequally  deep.  The  angle 
of  Louis  forms  a  prominent 
transsternal  ridge,  and  the 
ribs,  separated  by  unusu- 
ally wide  intercostal  spaces, 
incline  sharply  downward 
from  the  sternum  and  as 
sharply  bend  upward  again 

as  they  approach  the  spine.  The  subcostal  angle,  owing  to  this 
increased  obliquity  of  the  ribs,  is  extremely  acute.  The  shoulders 
generally  slope,  and  the  scapulae,  instead  of  hugging  the  back,  stand 
out  like  a  pair  of  wings — hence  the  term,  "winged"  or  "alar" 
scapulas.  The  chest  showing  the  foregoing  group  of  changes  has 
also  been  labeled  the  "expiratory  form  of  thorax." 

The  phthisical  thorax  must  not  be  mistaken  for  the  emaciated 
chest  of  a  patient  convalescent  from  some  acute  febrile  disease, 
such  as  enteric  fever;  in  the  latter  instance,  while  the  emaciation  of 
the  thoracic  parietes  may  be  striking,  the  chest  does  not  show  the 
slightest  evidence  of  actual  structural  deformity. 

The  Emphysematous  Thorax  (Inflated,  Barrel-chest). — The 
thorax  of  hypertrophic  (large-lunged)  emphysema  is  short,  deep, 
overdistended,  and  frequently  bulged  out  in  the  central  portion,  so 
that  it  conforms  more  or  less  to  the  shape  of  a  cask — the  so-called 


Fig.  24. — The  thorax  of  incipient  phthisis  (Jef- 
ferson Hospital). 


EXAMINATION    OF    THE    THORAX 


79 


"barrel-chest"   (Fig.  27).     This  peculiarity  is  most  striking  when 
the  emphysematous  enlargement  affects  especially  the  upper  pul- 


Fig.  25. — The  thorax  of  advanced  phthisis  (Philadelphia  General  Hospital). 

monary  lobes,  being  less  evident  when  the  process  is  diffuse  and  when 
it  implicates  chiefly  the  lower  part  of  the  lungs.  Fig.  20,  shows  a 
transverse  section  of  the  typical  "barrel  chest." 

The  neck  is  usually  short  and  thick, 
and  the  shoulders  elevated,  squarely  set, 
and  bent  forward.  The  angle  of  Louis 
is  prominent,  the  sternum  distinctly  pro- 
truded, and  the  upper  intercostal  spaces 
widened,  while  those  of  the  lower  thorax 
are  narrowed  and  drawn  in  during  in- 
spiration. The  ribs  run  horizontally 
from  the  sternum,  and  in  consequence 


Fig.  26. — Transverse  section  of 
a  phthisical  thorax. 


the  subcostal  angle  is  obtuse.     The  respiratory  movements  of  the 
emphysematous  chest  are  highly  characteristic,  the  excursion  being 


8o 


PHYSICAL    DIAGNOSIS 


vertical  and  rigid,  as  if  all  the  structures  of  the  thorax  were  welded 
together  and  rose  and  fell  en  masse. 

The  "inspiratory  form  of  chest"  is  a  term  also  applied  to  a  thorax 
having  these  characteristics,  and  the  presence  of  such  a  deformity 
is  almost  proof  positive  of  hypertrophic  pulmonary  emphysema, 
although  it  must  be  borne  in  mind  that  these  changes  do  not  neces- 


Fig.  27. — Emphysematous  thorax  (Philadelphia  General  Hospital). 

sarily  develop  in  every  case.  Kyphosis  may  superficially  resemble 
the  "barrel  chest,"  but  in  ordinary  "hump-back"  the  costosternal 
peculiarities  and  the  vertical  type  of  chest  movements  are  absent. 

The  Thorax  of  Atrophic  Emphysema. — This  is  the  small,  con- 
tracted type  of  chest  met  with  in  subjects  of  atrophic  (small-lunged) 
emphysema,  and  is  the  direct  consequence  of  senile  atrophy  of  the 
lungs.  The  thorax  is  abnormally  diminutive,  shallow,  and  peculiarly 


EXAMINATION    OF    THE    THORAX 


8l 


deformed  by  bowing  of  the  shoulders,  by  depression  of  the  sternum, 
clavicles,  and  ribs,  by  exaggerated  costal  obliquity,  and  by  narrow- 
ing of  the  lower  interspaces.  The  respiratory  excursion  is  greatly 


__      .J 

Fig.  28. — The  thorax  of  atrophic  emphysema  (Jefferson  Hospital). 


restricted,  for  the  chest-wall  is  rigid,  and  inspiratory  sucking  in  of 
the  supraclavicular  and  the  intercostal  spaces  may  occur.  The 
musculature  of  the  chest  is  generally  wasted 
and  flabby,  in  keeping  with  the  other  marks 
of  senility  shown  by  the  patient. 

The  Rachitic  Thorax. — In  rickets  the 
causes  of  the  chest  deformity  are  threefold: 
direct  muscular  action  upon  the  soft  bony 
structures,  pressure  upon  these  parts  by  the 
enlarged  viscera,  and  the  influence  of  atmos- 
pheric pressure.  These  combined  factors 
tend  to  produce  lateral  compression,  with 
relative  increase  in  the  anteroposterior  diam- 
eter of  the  thorax,  and  to  favor  the  formation  of  various  local 
flattenings,  prominences,  depressions,  and  lineal  markings  upon  its 


Fig.  29. — Transverse 
section  of  an  emphysem- 
atous  thorax. 


82  PHYSICAL   DIAGNOSIS 

surface.     Fig.  31  illustrates  a  cross-section  of  a  common  type  of 
rachitic  chest. 

The  most  distinctive  single  sign  of  rickets  is  the  so-called  rachitic 
rosary,  which  consists  of  a  beaded  line  paralleling  each  sternal  border 


Fig.  30. — The  rachitic  thorax  (Jefferson  Hospital). 

and  corresponding  to  the  course  of  the  chondrosternal  articulations. 
This  double  line  of  prominences,  due  to  thickening  of  the  costal 
cartilages,  is  to  be  felt  in  almost  every  rickety  child,  and  in  advanced 
cases  it  is  also  clearly  recognizable  on  inspection.  Another  important 
sign  of  rickets,  and  one  scarcely  less  characteristic  than  the  rosary, 
is  an  apparent  shortening  of  the  clavicles,  with  a  marked  exaggeration 
of  their  curves.  Prominence  of  the  thoracic  spine  (kyphosis)  is  a 
familiar  type  of  vertebral  deformity,  and 
frequently  the  vertebral  column  is  bent  for- 
ward (lordosis)  and  twisted  laterally  (sco- 
liosis)  (Fig.  32).  In  some  cases  the  spine 
remains  flexible,  but  in  others  it  is  found 
to  be  fixed  and  rigid.  The  vertebrae  may 
or  may  not  be  thickened,  and  sometimes  they 
are  studded  with  sharply  pointed,  conspicuous 
spinous  processes. 
The  pigeon-breast  (chicken-breast;  pectus  carinatum;  keel 
breast)  is  a  common  type  of  deformity  met  with  in  advanced  rickets 
(Fig.  33).  The  anteroposterior  diameter  of  the  chest  is  unduly 
increased,  the  lateral  thoracic  walls  are  compressed,  the  sternum  is 
pushed  forward  so  that  it  projects  like  the  keel  of  a  ship,  owing  to 


Fig.  31. — Transverse 
section  of  a  rachitic 
thorax. 


EXAMINATION    OF    THE    THORAX  83 

the  stress  upon  the  flexible  chondrosternal  joints  (Fig.  34).     The 


Fig.  32. — Thoracic  deformity  due  to  spinal  curvature  (Jefferson  Hospital). 

lower  margins  of  the  ribs  are  often  distended  or  flared  outward,  partly 
by  the  intra-abdominal  pressure  exerted  by  such  factors  as  ascites, 
tympanites,  and  enlarged  liver  and  spleen,  and 
partly  by  the  traction  of  the  diaphragm.  A 
transverse  groove,  or  furrow,  extending  from 
either  side  of  the  ensiform  cartilage  and  curv- 
ing downward  and  outward  toward  the  axilla? 
is  also  found  in  most  cases  of  rickets;  this 
furrow  corresponds  approximately  to  the  in- 
sertion of  the  diaphragm,  and  is  known  as 
Harrison's  sulcus  or  furrow. 

The  funnel -breast  (Trichterbrust ;  pectus  excavatum)  is  also 
sometimes  found  in  rickets,  especially  when  adenoid  and  tonsillar 


Fig.  33 . — Transverse 
section  of  a  pigeon- 
breast. 


54  PHYSICAL   DIAGNOSIS 

hypertrophies  coexist.  It  is  characterized  by  a  depression  of  the 
lower  part  of  the  sternum,  extending  from  the  tip  of  the  xiphoid, 
perhaps  as  high  as  the  middle  of  the  gladiolus.  This  deformity  is 
not  essentially  rachitic,  for  it  may  be  congenital,  secondary  to  non- 
rachitic  diseases,  or  acquired  as  the  result  of  pressure  upon  the  lower 
sternum.  The  funnel-breast  of  the  cobbler  (Schusterbrust),  due  to 
constant  pressure  of  the  last  against  the  lower  part  of  the  sternum, 


Fig.  34- — The  pigeon-breast  (Jefferson  Hospital). 

shows  a  concavity  limited  to   the  lower  gladiolus   and  to  the 
ensiform,  if  not  to  the  latter  process  alone  (Fig.  35). 

The  Flat  Thorax. — This  type  of  thorax  is  shallow  and 
broad,  although  the  length  is  not  abnormally  increased.  It 
is  distinguished  chiefly  by  the  conspicuous  flatness  and  breadth 
of  the  anterior  chest-wall  and  by  the  absence  of  the  normal 


EXAMINATION    OF    THE    THORAX  85 

forward  curve  of  the  ribs,  but  the  structural  peculiarities  of 
the  phthisical  thorax,  noted  above,  are  lacking.  To  be  flat- 
chested  does  not  necessarily  condemn  one  to  phthisis,  but  it  is 
at  least  suggestive  of  a  predisposition  to  this  disease. 

The  Fusiform  Thorax. — Habitual  tight  lacing  narrows  and 
elongates  the  thorax,  immobilizes  the  lower  ribs,  and  contracts 
their  intercostal  spaces.  In  consequence  of  this  compression 


Fig.  35-— Funnel-breast,  due  to  the  pressure  of  a  cobbler's  last  (Philadelphia  General 

Hospital). 

of  the  lower  thorax  the  chest  loses  its  normal  conic  shape, 
and  is  molded  into  a  more  or  less  iusiform  or  spindle-shaped 
structure,  the  waist-line  decreases  in  circumference,  and  is  low- 
ered at  the  expense  of  the  flanks,  the  vertical  extent  of  which 
is  considerably  lessened.  Exaggerated  upper  thoracic  breath- 
ing, upward  displacement  Df  the  thoracic  organs,  ptosis  of  the 
abdominal  viscera,  and  atrophy  of  the  spinal  muscles  are  the 
principal  structural  changes  which,  in  the  extreme  instance,  may 
result. 


86  PHYSICAL    DIAGNOSIS 

The  Boat-shaped  Thorax. — In  syringomyelia  there  may  be 
noted  a  median  depression  of  the  upper  anterior  wall  of  the 
thorax,  extending  as  far  downward  as  the  level  of  the  fifth 
rib.  The  chest,  hollowed  out  in  this  manner,  has  been  termed 
the  "  thorax  en  bateau  "  by  Marie,  from  its  rude  resemblance  to 
a  boat. 

The  Thorax  of  Progressive  Muscular  Atrophy. — In  the  adult 
this  myopathy  may  account  for  a  most  singular  deformity,  the  thorax 
being  converted  into  a  roughly  box-shaped  structure  whose  per- 
pendicular walls  project  some  distance  beyond  the  surface  of  the 
flanks,  which  are  immoderately  concave.  The  waist,  having  an 
atrophied  musculature,  contrasts  strikingly  with  the  contour  of  the 
chest,  and  appears  abnormally  constricted  and  slender — the  "taille 
de  guepe"  ("wasp  waist")  of  Landouzy  and  other  French  writers. 
Other  hall-marks  of  this  type  of  thorax  are  loss  of  the  normal  curve 
of  the  chest-walls,  extraordinary  obliquity  of  the  ribs,  especially  at 
the  base,  where  their  course  is  almost  vertical,  and  general  wasting 
of  the  thoracic  muscles. 

The  Gutter-chest. — As  the  result  of  antenatal  and  postnatal 
developmental  defects  the  chest  may  be  disfigured  by  the  presence  of 
a  narrow,  shallow,  vertical  gutter  or  groove  corresponding  to  the 
median  line  of  the  sternum.  This  peculiarity,  dubbed  the  "thorax 
en  gouttiere"  (Fere";  Schmidt),  is  due  to  an  exaggerated  forward 
convexity  of  the  costal  cartilages,  owing  to  which  their  sternal  extrem- 
ities are  closely  approximated  and  the  sternum  pressed  backward 
so  as  to  form  a  narrow  longitudinal  median  furrow. 

LOCAL  ASYMMETRY  OF  THE  THORAX 

Aside  from  the  foregoing  bilateral  thoracic  deformities,  there  are 
various  defects  of  contour  that  may  affect  either  one  entire  side  or 
a  circumscribed  area  of  the  chest.  The  anomalies  due  to  lesions 
of  the  thorax  and  of  the  upper  abdomen,  described  in  the  four  groups 
given  below,  are  to  be  distinguished  from  those  secondary  to  disease 
of  the  spine,  the  consideration  of  which  belongs  to  the  subject  of 
orthopedic  surgery. 

Unilateral  Bulging  (Fig.  36). — Enlargement  of  one  side  of  the 
thorax  generally  produces  a  leveling  or  a  bulging  of  the  intercostal 
spaces  on  the  affected  side;  indeed,  this  obliteration  of  the  inter- 
spaces may  exist  alone,  and,  if  so,  carries  practically  the  same  sig- 
nificance as  an  actual  overdistention  of  the  chest.  Fig.  37  shows 


EXAMINATION    OF   THE    THORAX 


the  outline  of  this  type  of  thoracic  deformity.     One-sided  distention 
is  met  with  in  large  pleural  effusions,  in  pneumothorax,  in  neoplasms 


Fig.  36. — Unilateral  enlargement  of  the  thorax  (Jefferson  Hospital). 

of  the  lung  and  the  pleura,  and  in  compensatory  emphysema  of  the 
lungs  secondary  to  lesions  of  the  opposite  side.     If  due  to  this  last 


Fig.  37. — Transverse  section  of  a  unilaterally  enlarged  thorax. 

cause,  the  contrast  between  the  two  halves  of  the  chest  is  espe- 


88  PHYSICAL   DIAGNOSIS 

dally  striking,  for  here  the  emphysematous  distention  is  brought 
into  comparison,  not  with  a  normal  opposite  side,  but  with  a 
shrunken,  diseased  one. 

Unilateral    Contraction   (Fig.   38).— Unilateral  flattening  or 
contraction  of  the  chest,  if  extensive,  causes  lowering  of  the 


Fig.  38. — Unilateral  retraction  of  the  thorax  due  to  empyema  (Jefferson  Hospital). 

shoulder  and  narrowing  of  the  intercostal  spaces  on  the  affected 
side,  together  with  more  or  less  spinal  curvature  and  twisting 
in  this  direction.  The  contracted  side  is  smaller  than  normal, 
while  the  opposite  side  is  often  found  to  be  vicariously  enlarged 


Fig-  3Q- — Transverse  section  of  a  unilaterally  retracted  thorax. 

(Fig.  39).  Chronic  pulmonary  tuberculosis,  interstitial  pneu- 
monia, wide-spread  pleural  adhesions,  and  chronic  compression 
of  the  lung  by  pleural  effusions  are  the  most  important  factors 
of  this  sort  of  deformity.  In  rare  instances  unilateral  contrac- 
tion of  the  thorax  may  arise  from  pulmonary  collapse  due  to  the 
obstruction  of  a  main  bronchus  by  a  tumor  or  by  a  foreign  body. 


EXAMINATION    OF    THE    THORAX 


Circumscribed  Prominences. — Local  swellings  or  prominences 
upon  the  chest-wall,  attributable  to  a  wide  range  of  causes,  are 
seen  most  commonly  upon  the  anterior  surface,  but  they  are  by  no 
means  restricted  to  this  part  of  the  thorax.  Bulging  in  the  cardiac 
region  (Fig.  40)  may  mean  enlargement  of  the  heart,  pericardial 
effusion,  pneumopericardium,  or  forward  dislocation  of  the  heart 
by  the  pressure  of  an  aneurism  or  a  new-growth.  It  is  in  young 
children  that  bulging  of  this  part  of  the  chest  is  most  frequent  and 
most  noticeable.  Aneurism  of  the  aortic  arch,  by  a  process  of  ero- 
sion, may  push  through  the  overlying  structures  and,  in  course  of 
time,  cause  a  local  tumor,  simulated,  at  least  superficially,  by  an 


L 


Fig.  40. — Precordial  bulging  due  to  cardiac 
hypertrophy  (Jefferson  Hospital). 


Fig  4L — Sternal  bulging  due  to  aneurism 
of  the  aortic  arch  (Jefferson  Hospital). 


abscess  of  the  soft  parts  or  by  the  simple  irregularity  in  the  contour 
of  the  sternal  or  the  costochondral  surfaces  (Fig.  41).  It  is  also 
possible,  at  first  glance,  to  mistake  an  aneurism  of  the  descending 
aorta  for  a  left  lateral  twist  of  the  spinal  column.  By  pressure,  a 
greatly  enlarged  liver  may  produce  decided  distention  of  the  lower 
right  thorax,  while  a  splenic  tumor  may  similarly  bulge  the  left  side 


PHYSICAL   DIAGNOSIS 


(Fig.  42).  Hypertrophy  of  the  breast  in  a  male  adolescent  (Fig.  43) 
is  a  curious  anomaly  sometimes  encountered.  As  already  noted, 
the  clavicles  and  the  scapulae  stand  out  prominently  in  the  phthisical 
thorax.  Prominence  of  either  scapula  may  be  caused  by  a  scoliosis 
and  by  paralysis  of  the  serratus  magnus  muscle,  while  the  left  scapula 
may  be  tilted  outward  by  the  backward  erosion  of  a  large  aneurismal 
dilatation  of  the  descending  thoracic  aorta.  Tumors  of  the  chest- 
wall,  the  lungs,  and  the  pleura,  empyema  necessitatis,  pulsating 
pleurisy,  tuberculous  disease  of  the  bony  thorax,  mediastinal  and 
subphrenic  abscesses,  and,  rarely,  hernia  of  the  lung,  are  also  cap- 
able of  pushing  out  the  chest-wall  within  a  restricted  area.  An 
encysted  pleural  effusion,  while  it  causes  no  local  bulging,  may 
obliterate  the  intercostal  spaces  over  its  site.  Myxedema  may  account 


Fig  42. — Thoracic  and  abdom- 
inal enlargement  due  to  splenic 
tumor  (Jefferson  Hospital). 


Fig.  43 — Hypertrophy  of  the  left  breast  in 
a  male  adolescent  (Jefferson  Hospital). 


for  supraclavicular  fibrofatty  deposits — Verneuil's  pseudolipomata. 
Subcutaneous  emphysema  is  recognized  as  a  gaseous,  crackling  swell- 
ing which  tends  to  disappear  by  absorption,  and  which  is  secondary 
to  the  rupture  of  some  air-containing  organ,  or  to  a  penetrating 
wound. 

Local  Depressions. — The  principal  intrathoracic  factors  of  local 
depressed  and  flat  areas  upon  the  surface  of  the  thorax  are  apical 


tuberculosis,  circumscribed   pleural   adhesions,  and   superficially 
seated  pulmonary  cavities.     (See  Figs.  24,  45,  46.)    Among  other 


Fig.  44. — Lateral  compression   of  the        Fig.  45. — Local  retraction  of  the  thorax  due 
thorax  {Jefferson  .Hospital).  to  pulmonary  fibrosis  and  pleurisy  (Jefferson 

Hospital). 

causes  of  such  deformities  may  be  mentioned  atelectasis,  bronchiec- 
tasis,  fractured  ribs,  cicatrices  consequent  to  rib  resection  and  to 


Fig.  46. — Transverse  section  of  a  locally  retracted  thorax. 

healed  empyema  necessitates,  and  atrophy  or  removal  of  a  breast 
or  of  the  musculature  of  the  chest- wall. 


Q2  PHYSICAL    DIAGNOSIS 

RESPIRATORY  MOVEMENTS  OF  THE  THORAX 

The  student  must  become  familiar  not  only  with  normal  respiratory 
movements  of  the  chest,  but  also  with  the  abnormalities  of  breathing 
symptomatic  of  pathologic  conditions.  This  information  is  acquired 
by  observing  the  frequency,  the  rhythm,  and  the  type  of  the  thoracic 
movements,  the  degree  and  character  of  the  chest  expansion,  and  the 
extent  and  freedom  of  the  diaphragm  excursion.  The  adequacy  of 
blood  oxygenation,  as  shown  by  the  color  of  the  patient,  is  an  inti- 
mate correlative  of  these  signs,  with  which  it  will  be  considered 
below. 

Normal  Respiratory  Movements. — The  respiratory  cycle  con- 
sists of  an  active  inspiratory  effort  and  a  passive  expiratory  phase, 
followed  by  a  pause,  the  relative  duration  of  the  two  movements 
being  thus  expressed  :  inspiration  :  expiration  :  :  5  :  6.  The  respira- 
tory-pulse ratio  averages  about  1:4.  In  adults  the  normal  respiratory 
frequency  is  from  1 6  to  24  to  the  minute  (Hutchinson) ,  while  in  children 
the  average  ranges  from  44  in  the  new-born  to  26  in  the  five-year-old 
child  (Quetelet).  Normal  breathing  is  usually  regular  and  quiet, 
but  its  rhythm  and  tranquillity  may  be  deranged  by  mental  disturb- 
ances, by  muscular  exertion,  and  by  fatigue.  The  respirations  may 
be  timed  either  by  simply  watching  the  chest  movements  or  by  pal- 
pation, with  the  hand  applied  to  the  lower  part  of  the  thorax. 

The  movements  of  the  two  sides  of  the  chest  are  synchronous,  and, 
except  for  a  trifling  physiologic  overfulness  of  the  right  half,  prac- 
tically symmetric.1  Each  inspiration  increases  all  the  diameters  of 
the  chest,  and  is  attended  by  ascent  and  forward  projection  of  the 
sternum,  by  ascent  and  eversion  of  the  ribs,  and  by  bulging  of  the 
upper  epigastrium;  with  expiration  the  decrease  in  the  chest  diameters 
is  accompanied  by  retrocession  of  the  parietes  and  by  reappearance 
of  the  normal  epigastric  hollow.  The  movements  of  inspiration 
are  performed  ordinarily  by  the  diaphragm,  intercostals,  scaleni, 
serrati  postici,  and  levatores  costarum;  but  extraordinary  efforts  in 
breathing  call  into  play  the  following  accessory  muscles:  pectorales, 
quadratus  lumborum,  serratus  magnus,  sternomastoid,  latissimus 
dorsi,  infrahyoid,  and  erector  spinae  (Cunningham).  The  move- 
ments of  expiration  are  due  principally  to  the  elasticity  of  the  lungs, 
the  ascent  of  the  diaphragm,  the  weight  of  the  chest-wall,  and,  in 
difficult,  forceful  deflation  of  the  lungs,  to  the  auxiliary  action  of  the 
intercostal,  triangularis  sterni,  and  upper  abdominal  muscles. 

1  Most  women,  according  to  Ransome,  show  a  greater  respiratory  movement 
of  the  left  side  of  the  chest. 


EXAMINATION    OF    THE    THORAX 


93 


The  type  of  respiration  differs  normally  in  the  two  sexes,  and  is  also 
influenced  by  the  age  of  the  individual.  Thus,  in  women  costal  or 
thoracic  breathing  is  the  rule,  which  means  that  respiration  is  carried 
on  chiefly  by  the  upper  part  of  the  thorax,  the  scaleni  and  the  upper 
intercostals  being  actively  brought  into  play  and  the  sternum  and 
upper  ribs  conspicuously  elevated  and  projected,  while  the  epigas- 
trium remains  immobile,  or,  at  the  most,  moves  but  moderately. 
In  men  and  in  children  of  both  sexes,  on  the  contrary,  respiration 
is  of  the  abdominal  or  diaphragmatic  type,  being  performed  mainly 
by  the  action  of  the  lower  part  of  the  thorax  and  of  the  diaphragm, 
whose  descent  causes  bulging  of  the  epigastrium  during  inspiration. 


Fig.  47 — Technic  of  determining  Litten's  diaphragm  sign. 

In  women  of  advanced  age,  whose  chests  have  become  rigid  and 
fixed,  more  or  less  tendency  toward  abdominal  respiration  is  also  seen. 
The  Diaphragm  Phenomenon. — The  normal  inspiratory  descent 
of  the  diaphragm  is  recognized  as  a  faint,  although  perfectly  apprecia- 
ble, shadow  which  travels  vertically  down  the  lower  axilla  during  each 
full  inflation  of  the  lungs,  from  the  sixth  to  the  eighth  or  ninth  inter- 
costal spaces.  This  so-called  diaphragm  phenomenon  (Litten's  sign) 
is  shown  most  distinctly  by  placing  the  subject  in  dorsal  decubitus, 
with  the  feet  toward  a  window  and  the  arms  extended  above  the 
head,  the  observer  standing  behind  or  at  the  side  of  the  bed,  in  the 
position  indicated  by  the  accompanying  picture  (Fig.  47).  The 
shadow,  which  ordinarily  has  a  vertical  course  of  three  .or  four  inches 


94  PHYSICAL   DIAGNOSIS 

with  each  deep  inspiration,  is  explained  by  the  inspiratory  separation 
of  the  diaphragm  from  the  thoracic  wall,  an  act  that  increases  the 
extent  of  the  complementary  pleural  sinus  and  exerts  suction  upon 
the  intercostal  spaces  below  the  inferior  border  of  the  lung. 
Naturally,  the  diaphragm  shadow  is  virtually  imperceptible  during 
expiration. 

Litten's  sign  is  present  in  practically  every  healthy  individual, 
except  in  those  who  are  overmuscular  or  overfat,  and  it  shows  that 
the  excursions  of  the  diaphragm,  the  lung,  and  the  pleura  are  unre- 
stricted. Conditions  interfering  with  such  movements  partly  or 
entirely  abolish  the  diaphragm  shadow  upon  the  affected  side,  as  is 
the  case  in  pleural  adhesion  and  effusion,  basal  pneumonia,  extensive 
emphysema,  pneumothorax,  and  neoplasms  of  the  lower  part  of  the 
thoracic  cavity.  To  some  extent  subdiaphragmatic  abscess,  enlarge- 
ment of  the  liver  and  of  the  spleen,  and  extreme  distention  of  the 
abdomen  by  fluid,  gas,  or  solid  tumors  act  in  a  similar  manner,  while 
in  many  cases  of  incipient  phthisis  the  shadow  is  more  or  less  inde- 
finable. In  paralysis  of  the  diaphragm  the  phenomenon  is  totally 
abolished,  and  in  persons  whose  chest  expansion  is  restricted  the 
sign  is  difficult  of  detection.  The  presence  of  edema  of  the  chest- 
wall  effectually  obscures  the  phrenic  shadow. 

Respiratory  Alterations  of  the  Subcostal  Angle. — The  study  of 
the  diaphragm  shadow  should  always  be  supplemented  by  de- 
termining the  presence  of  any  unnatural  change  in  the  subcostal 
angle,  as  shown  by  Hoover's  method  of  combined  inspection  and 
bimanual  palpation  with  the  thumbs  symmetrically  placed  along 
the  costal  borders  to  serve  as  indicators  of  their  divergence  from, 
or  convergence  toward,  the  median  line.  This  simple  maneuver 
shows  that  with  an  identical  limitation  of  inspiratory  excursions, 
in  both  basal  pneumonia  and  in  pleural  effusion,  there  is  diverg- 
ence of  the  costal  borders  in  the  former  and  convergence  in  the 
latter.  In  pleural  adhesion  simple  restriction  is  the  rule,  without 
definite  change  in  the  subcostal  angle.  Inspiratory  divergence, 
with  consequent  widening  of  the  subcostal  angle,  is  observed  in 
paralysis  of  the  diaphragm,  in  subphrenic  abscess,  and  in  hepatic 
enlargement,  while  in  emphysema,  in  pneumothorax,  and  in  large- 
sized  pericardial  effusion  the  reverse  occurs.  In  the  foregoing  the 
respiratory  changes  noted  correspond  to  the  affected  side.  Cardiac 
enlargements  may  alter  the  respiratory  excursion  of  either  the  left 
costal  margin  or  of  both  borders,  the  left  being  affected  in  left- 
sided  enlargements,  and  both,  with  symmetric  narrowing  of  the 
subcostal  angle,  in  an  enlargement  in  the  median  line,  as  commonly 
occurs  in  mitral  stenosis. 


EXAMINATION    OF   THE    THORAX  95 

Unlike  Litten's  diaphragm  phenomenon,  the  movements  of  the 
costal  borders  are  not  obscured  by  either  a  thick  layer  of  fat  or 
by  muscular  overdevelopment  of  the  subject,  and,  therefore,  their 
study  deserves  wide  clinical  application  in  the  differentiation  of 
lesions  of  the  lower  thorax  and  of  the  upper  abdomen. 

ANOMALIES   OF    RESPIRATION 

Under  this  caption  are  included  the  various  disturbances  of  the 
respiratory  excursion  distinguished  chiefly  by  deviations  from  its 
normal  extent,  frequency,  and  rhythm. 

Reversal  of  the  Respiratory  Type. — Costal  breathing  in  a  man 
and  abdominal  breathing  in  a  woman,  being  just  the  reverse  of  the 
respiratory  type  normally  occurring  in  the  two  sexes,  are  to  be  regarded 
as  distinctly  anomalous.  Exaggeration  of  the  type  of  breathing 
peculiar  to  either  sex  is  to  be  interpreted  in  the  same  light. 

Costal  breathing  is  associated  with  conditions  that  restrict  the 
movements  of  the  diaphragm,  such  as  diaphragmatic  pleurisy  and 
paralysis,  extensive  pericardial  effusion,  emphysema,  ascites,  tympan- 
ites, abdominal  tumor,  and  peritonitis.  Exaggeration  of  the  respir- 
atory movements  of  the  upper  thorax  attends  various  forms  of  dyspnea, 
notably  those  of  hysteric  origin. 

Abdominal  breathing,  prevailing  because  of  some  mechanical  im- 
pediment to  the  free  movements  of  the  chest,  occurs  in  bilateral 
pleural  effusion,  in  massive  pneumonia,  in  calcareous  disease  of 
the  chest-wall,  and  in  scleroderma.  Spinal  paralysis,  tetanus,  and 
strychnin  poisoning  also  throw  the  work  of  the  thoracic  movements 
upon  the  abdomen.  The  conditions  noted  below  as  factors  of 
deficient  expansion,  owing  to  the  painful  breathing  they  excite,  also 
favor  more  or  less  the  abdominal  type  of  respiration. 

Sternomastoid  Breathing. — Undue  contraction  of  the  sternomastoid 
muscles  is  noticeable  whenever  the  respiratory  function  suffers  any 
extraordinary  stress,  and,  therefore,  such  action  is  a  common  sign 
in  most  forms  of  dyspnea  (q.  v.).  So  conspicuous  are  the  contrac- 
tions of  this  muscular  group  in  the  dying  state  that  this  action  has 
been  termed  a  "veritable  death's  call"  (R.  H.  Chase). 

Alterations  in  the  Degree  of  Expansion. — A  general  defi- 
ciency in  the  expansion  of  the  chest,  or  shallow  breathing,  may  be 
simply  a  personal  peculiarity,  and  hence  is  without  definite  import; 
more  often,  however,  it  is  suggestive  of  either  latent  or  active  pul- 
monary tuberculosis,  especially  if  flat-chestedness  coexists.  Feeble 
expansion  is  perhaps  best  illustrated  by  the  thoracic  immobility 


96  PHYSICAL   DIAGNOSIS 

incident  to  such  conditions  as  collapse,  acute  syncope,  trance,  and 
the  adynamia  of  acute  febrile  diseases.  The  overdistended  thorax 
of  the  emphysematous  subject  can  expand  but  slightly,  and  the 
mobility  of  the  chest  is  impaired  by  laryngeal  or  tracheal  stricture, 
and  by  paralysis  or  spasm  of  the  respiratory  muscles  and  of  the 
diaphragm.  Deficient  chest  expansion  from  ossification  of  the  costal 
cartilages  (Bryson's  sign)  often  occurs  in  Graves'  disease.  Painful 
breathing  limits  the  respiratory  excursion,  which  is  restricted  for 
this  reason  in  pleurisy,  pericarditis,  peritonitis,  intercostal  neuralgia, 
rheumatism,  and  diseases  of  the  chest-wall. 

Wavy  and  uneven  expansion,  or  a  peculiar  undulatory  type  of 
respiratory  movements,  frequently  develops  during  the  adynamia  of 
the  so-called  "typhoid  state." 

Deficient  expansion  and  inspiratory  retraction  of  the  interspaces 
sometimes  coexist,  as  in  stenosis  of  the  upper  air-passages  and  in 
diffuse  bronchopneumonia,  in  which  conditions  inflation  of  the  lungs 
is  performed  with  great  difficulty.  Retraction  of  the  lower  inter- 
spaces with  a  simultaneous  bulging  in  the  supraclavicular  regions 
is  a  distinctive  finding  in  advanced  emphysema.  Bronchial  stenosis, 
atelectasis,  and  pleural  adhesion  are  factors  of  unilateral,  and  of 
limited,  circumscribed  intercostal  retraction. 

Unsymmetric  expansion,  characterized  by  a  one-sided  deficiency 
of  the  respiratory  movements,  is  commonly  met  with  in  conditions 
that  mechanically  interfere  with  the  movements  of  the  affected  lung — 
pleural  effusion,  wide-spread  pleural  adhesion,  massive  pneumonia, 
pneumothorax,  and  tumor  of  the  lung;  while  a  lung  crippled  by 
tuberculosis,  by  cirrhosis,  or  by  atelectasis  also  fails  to  inflate  and 
deflate  normally.  Either  a  foreign  body  lodged  in  a  main  bronchus 
or  a  tumor  constricting  its  lumen  can  account  for  unilateral  interfer- 
ence with  expansion  on  the  side  implicated.  Right-sided  restriction 
of  breathing  may  be  symptomatic  of  hepatic  enlargement,  and  left- 
sided,  of  hypertrophied  spleen. 

Circumscribed  deficiency  of  expansion,  showing  as  a  local  patch  of 
immobility  upon  the  chest-wall,  is  significant  of  some  limited  lesion 
of  the  lung,  pleura,  or  pleuropericardium.  Immobility  and  lagging 
in  an  infraclavicular  space  suggests  tuberculosis,  pneumonia,  or 
adhesive  pleurisy  in  this  region;  if  it  affects  the  lower  part  of  the 
thorax,  basal  pneumonia  or  diaphragmatic  pleurisy  is  to  be  thought 
of;  and  if  it  be  localized  in  the  region  of  the  heart,  pericardial  adhe- 
sions are  to  be  suspected. 

A  general  increase  in  the  expansion  of  the  chest  occurs  as  the  physio- 
logic effect  of  hard  exercise,  attends  various  emotional  states,  and  is 


EXAMINATION    OF    THE    THORAX  97 

seen  in  certain  forms  of  dyspnea.  The  vicarious  overaction  of  one 
lung  or  of  a  part  of  one  lung  is  the  underlying  cause  of  a  unilateral 
or  circumscribed  increase  in  expansion. 

Alterations  in  the  Frequency  of  the  Respiratory  Movements. — 
Simple  rapid  breathing,  or  polypnea,  usually  attended  by  shallowness 
of  the  respiratory  excursion,  occurs  normally  in  young  children,  and 
is  the  physiologic  result  of  active  exercise,  although  in  the  latter 
instance  the  breathing  is  deep,  as  well  as  rapid.  Accelerated  respira- 
tion is  also  met  with  in  neurotics,  in  many  of  the  acute  fevers,  and  in 
pulmonary  lesions,  such  as  pneumonia  and  tuberculosis,  which  not 
only  diminish  the  aerating  surface  of  the  lungs,  but  also  elaborate 
toxins  that  probably  stimulate  the  respiratory  center. 

Slow  breathing,  or  oligopnea,  occurs  in  many  conditions  of  coma, 
collapse,  and  shock  from  various  causes ;  in  cerebral  tumor,  apoplexy, 
and  meningitis;  in  poisoning  by  opium,  chloral,  chloroform,  aconite, 
and  antimony;  and,  occasionally,  in  bronchial  asthma.  The  associa- 
tion of  arythmic  and  difficult  respiration  is  discussed  under  Dyspnea 
(q.  -v.). 

Respiratory  Arhythmia. — Simple  irregularity,  often  temporary, 
in  the  rhythm  of  the  respiratory  movements  is  not  necessarily  patho- 
logic, since  it  is  often  referable  to  trivial  psychic  disturbances.  It  is, 
on  the  contrary,  a  sign  of  grave  import  in  apoplexy,  uremia,  menin- 
gitis, cerebral  tumor,  lesions  of  the  medulla,  and  in  states  of  collapse. 
Respiratory  arhythmia  may  also  accompany  chorea,  and  frequently 
is  found  in  pneumonia  and  in  atelectasis,  being  evidenced  in  these 
last  two  conditions  as  a  distinct  post-inspiratory  pause. 

Jerky  respiration,  characterized  by  a  series  of  spasmodic  interrup- 
tions of  inspiration  and  expiration,  is  in  some  instances  purely  hysteric, 
but  in  others  it  is  attributable  to  some  one  of  the  factors  of  restricted 
respiration  referred  to  in  a  preceding  paragraph.  (See  p.  95.) 
Chorea,  asthma,  hemiplegia,  and  rabies  are  additional  causes  of  this 
respiratory  peculiarity. 

Cheyne-Stokes  respiration  is  characterized  by  periodic  disturbances 
of  the  respiratory  rate,  rhythm,  and  volume,  alternating  with  intervals 
during  which  breathing  entirely  ceases,  these  two  contrasting  phases 
recurring  in  regular  cycles.  Thus,  one  of  these  quiescent  intervals 
(period  of  apnea)  is  followed  by  slow  and  shallow  respirations,  which 
progressively  increase  in  both  frequency  and  in  volume  until  they 
reach  an  acme  (period  of  dyspnea) ,  after  which  they  gradually  become 
slower  and  shallower  until,  having  ceased  entirely,  another  quiescent 
period  begins  (Fig.  48).  The  length  of  the  two  periods  is  variable — 
a  few  seconds  to  one  or  even  two  minutes  for  the  dyspneic  phase, 

7 


PHYSICAL   DIAGNOSIS 


and  as  long  as  one  minute  for  the  apneic.  Sighing  and  snoring 
sometimes  attend  the  deep  respiratory  efforts  just  preceding  the 
acme  of  dyspnea,  and  cyanosis  is  a  familiar  objective  symptom 
at  this  time.  The  difference  between  Cheyne-Stokes,  normal,  and 


Fig.  48. — Cheyne-Stokes  respiration;  upstroke:  inspiration;  downstroke:  expira- 
tion. The  small  waves  in  the  period  of  apnea  are  due  to  the  heart-beat  (Pneumo- 
gram  by  Dr.  G.  Bachmann). 

shallow  respiration  is  graphically  shown  by  Fig.  49.  It  is  of  some 
importance  to  recall  Eyster's  observation,  that  arterial  hyperten- 
sion accompanies  the  dyspneic  period  of  Cheyne-Stokes  respiration 
due  to  cerebral  compression,  while  in  that  due  to  cardiorenal  dis- 

vWWWWWW 


Shallow  • 


Fig.  49. — Normal  and  pathologic  types  of  respiration. 

ease  and  other  factors  the  blood-pressure  rises  during  the  apneic 
stage.  As  a  rule,  the  pulse-rate  appreciably  shows  during  apnea, 
but  in  some  cases  the  reverse  occurs. 

The  persistence  of  Cheyne-Stokes  respiration  ranges  from  a  few 
hours  to  as  long  as  several  weeks,  or,  in  the  extreme  case,  several 


EXAMINATION    OF    THE    THORAX  99 

months.  The  patient  sometimes  becomes  insensible  during  the 
phase  of  apnea,  but  regains  consciousness  as  breathing  is  resumed. 
This  type  of  respiration  also  may  occur  in  coma,  as  well  as  in 
ordinary  sleep. 

Cheyne-Stokes  respiration  invariably  has  a  grave,  although  not 
necessarily  a  fatal,  significance.  It  may  attend  almost  any  pro- 
foundly comatose  state,  but  its  presence  especially  suggests  factors 
such  as  apoplexy,  cerebral  tumor  or  softening,  meningitis,  uremia, 
diabetes  mellitus,  opium-poisoning,  and  fatty  heart  or  other  degen- 
erative cardiac  lesions.  With  less  frequency  it  is  observed  in  the 
typhoid  states  of  various  acute  infectious  diseases,  in  general  paral- 
ysis, and  as  the  result  of  embolism  and  of  hemorrhage.  Cheyne- 
Stokes'  respiration  is  due  to  diminished  irritability  of  the  respira- 
tory center,  but  whether  this  can  be  accounted  for  simply  by 
fatigue  (Rosenbach's  belief)  or  by  faulty  oxygenation  (Traube's 
view)  is  a  moot  point. 

Meningeal  respiration  consists  of  recurring  periods  of  apnea, 
ranging  from  five  or  ten  to  twenty  or  thirty  seconds'  duration,  and 
separated  by  intervals  marked  by  irregularity  of  rhythm  and  of 
force.  The  apneic  periods  recur  irregularly,  and  commonly  are 
preceded  or  succeeded  by  a  deep  sighing  respiration.  This  res- 
piratory anomaly,  also  known  as  Blot's  respiration,  is  particularly 
suggestive  of  meningitis,  but  it  may  be  symptomatic  of  the  same 
factors  to  which  typical  Cheyne-Stokes  respiration  is  referable. 

An  extraordinary  example  of  voluntary  apnea  in  a  young  athlete, 
who  held  his  breath  for  ten  minutes  and  ten  seconds,  is  recorded 
by  Saxton  Pope. 

Stertorous  respiration,  or  snoring,  caused  by  the  vibrations  of 
a  relaxed  soft  palate,  occurs  usually,  but  not  exclusively,  during 
either  sleep  or  coma.  It  is  a  well-known  sign  of  profound  sleep  in 
many  healthy  persons  who  sleep  with  their  mouth  open,  and  is  heard 
with  great  constancy  in  the  condition  known  as  "mouth-breathing," 
consequent  to  tonsillar  hypertrophy,  postnasal  adenoids,  quinsy, 
and  postpharyngeal  abscess,  the  noisy  snoring  of  this  last- 
named  condition  having  been  dubbed  the  "  hen-cluck  "  stertor.  Of 
the  more  serious  factors  of  stertorous  breathing,  one  should  remember 
paralysis  of  the  soft  palate,  and  the  comatose  states  of  uremia,  apo- 
plexy, diabetes  mellitus,  asphyxia,  opium-poisoning,  pulmonary 
edema,  epilepsy,  and  cerebral  compression. 

Stridulous  respiration,  denoting  stenosis  of  the  larynx  or  trachea, 
is  audible,  especially  during  inspiration,  as  a  medley  of  harsh,  hissing, 
or  whistling  vibratory  sounds,  the  production  of  which  is  due  to  some 
local  lesion  of  the  parts  or  to  a  primary  interference  with  the  functions 


100  PHYSICAL   DIAGNOSIS 

of  the  laryngeal  muscles.  Thus,  stridor  is  commonly  the  result  of 
inflammatory  turgescence,  edema,  diphtheria,  neoplasm,  and  of  a 
foreign  body  in  the  larynx  or  trachea.  Or  it  may  relate  to  the  laryn- 
geal spasm  of  spasmodic  croup,  laryngismus  stridulus  (child-crowing; 
thymic  asthma),  locomotor  ataxia  (laryngeal  crisis),  tetanus,  or 
strychnin-poisoning.  In  other  instances  irritation  of  the  inferior 
laryngeal  nerve  by  the  encroachment  of  an  aneurism,  a  neoplasm 
of  the  mediastinum  or  trachea,  a  mass  of  enlarged  bronchial  glands, 
or  a  dislocated  heart  is  the  exciting  cause  of  stridor.  Respiration 
through  a  tracheotomy  tube  produces  a  rasping  sound  not  unlike 
that  made  by  filing  the  teeth  of  a  saw — hence  the  term,  stridor 
serraticus.  The  stridor  of  tracheal  stenosis  is  also  known  as  the 
"leopard's  growl." 

DYSPNEA 

Dyspnea  means  difficult  or  labored  respiration,  and  these  laborious 
efforts  to  breathe  are  the  distinctive  hall-mark  of  the  sign,  irrespective 
of  any  coexisting  disturbances  of  the  respiratory  rate,  rhythm,  and 
depth.  When  dyspnea  is  striking,  the  respiratory  movements  are 
obviously  embarrassed,  as  shown  by  the  overaction  of  the  accessory 
muscles  of  respiration  upon  which  demand  is  made,  and  the  patient's 
anxious  face,  dilated  pupils,  moist  skin,  dry  tongue  and  lips,  gaping 
mouth,  dilated  alae  nasi,  and  cyanosis  constitute  a  very  distinctive 
clinical  picture  of  the  extreme  respiratory  distress.  When  the 
dyspnea  is  so  urgent  that  the  subject  can  breathe  only  when  in  an 
upright  position,  the  term  orthopnea  is  used. 

Labored  inspiration,  with  natural  expiration,  the  effort  here  being 
made  to  inflate  the  lungs,  is  known  as  inspiratory  dyspnea;  but  when, 
on  the  other  hand,  expiration  is  interfered  with,  the  effort  being  made 
to  deflate  the  lungs,  the  condition  is  one  of  expiratory  dyspnea.  When 
both  inspiration  and  expiration  are  labored, — and  this  is,  by  far, 
the  commonest  type, — the  term  mixed  dyspnea  is  employed.  Accord- 
ing to  the  nature  of  the  underlying  factor  or  factors,  dyspnea  is  either 
constant  or  paroxysmal.  When  the  patient  is  conscious  of  shortness, 
of  breath,  subjective  dyspnea  exists;  while  in  objective  dyspnea  the 
labored  breathing  is  apparent  to  the  examiner,  although  the  patient 
is  not  necessarily  distressed  thereby. 

Types  of  Dyspnea. — Aside  from  the  dyspnea  arising  from 
purely  functional  causes,  the  most  important  clinical  types  are  those 
attributable  to  anemia,  toxemia,  stenosis  of  the  air-passages,  and 
organic  lesions  of  the  lungs  and  the  cardiovascular  system.  These 
causes,  together  with  others  of  minor  interest,  may  be  considered 
briefly  under  the  following  headings. 


EXAMINATION    OF    THE    THORAX  IOI 

Functional  Dyspnea. — Any  form  of  active  muscular  exercise  may 
be  responsible  for  a  temporary  dyspnea  of  the  mixed  type,  such  as 
that  illustrated  by  the  labored,  deep,  and  hurried  breathing  of  the 
oarsman  after  a  hard  row,  or  of  the  sprinter  after  a  hundred  yards' 
dash.  Temporary  congestion  of  the  pulmonary  capillaries  best 
accounts  for  this  form  of  dyspnea,  though  it  may  be  true  that  there 
is  some  irritation  of  the  respiratory  center  by  circulating  toxins 
elaborated  by  abnormally  active  tissue  metabolism.  Trifling  exer- 
tion, insufficient  even  to  hurry  the  respiration  of  a  normal  person,  is 
often  sufficient  to  embarrass  seriously  the  breathing  of  those  affected 
with  incipient  phthisis,  imperfectly  compensated  cardiac  disease, 
chronic  bronchitis,  emphysema,  anemia,  and  obesity. 

The  functional  neuroses  account  for  a  similar  kind  of  dyspnea,  as 
in  persons  of  a  nervous  temperament,  especially  neurotic  and  hysteric 
women,  whose  shortness  of  breath  is  distressing  enough  to  amount 
to  an  actual  dyspnea,  despite  the  fact  that  no  more  tangible  cause 
than  simple  excitement  or  emotion  is  apparent.  Perverted  action 
of  the  respiratory  center  has  been  suggested  as  the  explanation  of  the 
dyspnea  in  such  cases. 

Anemic  Dyspnea. — In  high-grade  anemia  the  diminished  oxygen 
content  of  the  blood  leads  to  difficult  breathing  and  to  increased 
frequency  and  depth  of  the  respiratory  movements,  in  order  thus  to 
compensate  for  the  oxygen  deficiency  by  an  unusually  thorough  oxy- 
genization  of  all  the  available  hemoglobin.  The  degree  of  a  purely 
anemic  dyspnea  stands  in  direct  relation  to  the  extent  of  the  hemo- 
globin loss,  being  more  decided  in  pernicious  anemia,  in  chlorosis, 
and  in  acute  leukemia  than  it  is  in  the  ordinary  forms  of  secondary 
anemia.  Here  also  may  be  mentioned  the  dyspnea  due  to  the  breath- 
ing of  impure  air,  as  illustrated  by  the  form  of  respiratory  distress 
know  as  "mountain  sickness,"  caused  by  breathing  air  deficient  in 
oxygen,  and  by  the  extreme  dyspnea,  if  not  the  asphyxia,  of  coal-gas 
poisoning,  in  which  carbon  monoxid  replaces  the  oxygen  of  the 
circulating  blood. 

Toxemic  Dyspnea. — In  active  fevers  rapid,  difficult  breathing  is 
likely  to  develop  from  the  effect  of  the  attendant  toxemia,  as  well 
as  from  irritation  of  the  respiratory  center  by  abnormally  warm 
blood.  Uremic  dyspnea,  observed  in  the  nephritides,  may  be  a  sign 
of  uremic  intoxication,  but  it  also  must  be  referred  to  such  additional 
factors  as  cardiovascular  disturbances  and  to  inflammatory  and  me- 
chanical implication  of  the  bronchopulmonary  apparatus.  In  gen- 
eral, the  uremia  of  renal  disease  is  the  evidence  of  an  attempt  of  the 
lungs  to  compensate  the  existing  acidosis,  and  to  a  less  extent  it  is 


102  PHYSICAL    DIAGNOSIS 

a  sign  of  increased  excitability  of  the  respiratory  center.  So-called 
"renal  asthma"  is  an  unfortunate  term,  generally  confounded  with 
the  breathlessness  of  nephritis,  though  it  must  be  admitted  that  an 
occasional  instance  of  true  bronchial  asthma  is  possibly  of  uremic 
origin.  Renal  dyspnea  is  frequently  paroxysmal,  but  it  may  be  of 
a  continuous  type,  with  or  without  Cheyne-Stokes  breathing  and 
cyanosis.  Diabetic  dyspnea,  or  KussmauPs  air-hunger,  is  commonly 
of  the  mixed  type,  and  is  characterized  by  deep,  but  not  unduly 
rapid,  respiratory  excursions,  with  or  without  cyanosis.  It  frequently 
ushers  in  an  attack  of  diabetic  coma  during  which  it  may  become 
transformed  into  Cheyne-Stokes  respiration.  This  precomatose 
form  of  dyspnea  is  explained  partly  by  the  toxic  action  of  the  diabetic 
acidosis  and  partly  by  the  fact  that  the  oxygen  capacity  of  diabetic 
blood  is  subnormal.  Toxemia  plus  hemolytic  reduction  of  the  oxy- 
gen content  of  the  blood  is  the  credible  factor  of  the  dyspnea  incident 
to  malignant  jaundice,  hepatic  cirrhosis,  insolation,  and  the  malarial 
chill. 

Obstructive  and  Mechanical  Dyspnea. — It  is  convenient  here 
to  consider  the  varieties  of  respiratory  difficulty  symptomatic  of 
stenosis  of  the  air-passages,  of  mechanical  interference  with  the 
thoracic  movements,  and  of  spastic  or  paralytic  lesions  of  the 
respiratory  muscles. 

Stenosis  of  tlie  upper  air-passages,  in  that  it  obstructs  the  free 
entrance  of  air  to  the  lungs,  is  a  prominent  cause  of  inspiratory 
•dyspnea  characterized  by  slow,  deliberate,  deep  respiratory  efforts, 
which  tend  to  overcome  the  obstruction  much  more  effectually  than 
does  hurried,  shallow  breathing.  When  the  grade  of  stenosis  is 
so  extreme  that  the  efforts  of  inflation  actually  rarefy  the  pulmonary 
air,  inspiratory  retraction  of  the  lateral  walls  of  the  thorax  and  of  the 
epigastrium  is  noticeable,  and  the  lower  intercostal  spaces,  the  supra- 
sternal  notch,  and  the  supraclavicular  regions  are  sucked  in  with 
each  deep  breath.  Stridor,  as  noted  in  a  foregoing  paragraph,  is 
also  a  noteworthy  sign  of  stenosis  of  the  upper  air-passages.  Of 
the  conditions  responsible  for  respiratory  stenosis,  the  following 
are  important:  tonsillar  enlargement  and  retropharyngeal  abscess; 
membranous,  edematous,  and  inflammatory  occlusion  of  the  larynx; 
laryngismus  stridulus,  croup,  and  paralysis  of  the  dilators  of  the 
glottis;  and  stenosis  of  the  larynx,  trachea,  or  main  bronchus 
by  cicatrix,  foreign  body,  neoplasm,  glandular  enlargement,  or 
aneurism.  In  young  children  alarming  paroxysms  of  dyspnea 
and  respiratory  stridor  may  be  excited  by  the  pressure  of  a  thymus 
hyperplasia  upon  the  trachea. 


EXAMINATION    OF    THE    THORAX  103 

In  extreme  bronchial  obstruction  there  is  wide-spread  blocking  of 
the  bronchioles  by  swelling,  spasm,  or  exudate,  and  in  consequence 
rapid  breathing  and  urgent  expiratory  dyspnea  occur,  marked  by  great 
prolongation  of  expiration,  cyanosis,  and  perhaps  by  stridor.  This 
is  especially  prone  to  occur  in  the  diffuse  catarrhal  pneumonia  of 
young  children,  in  bronchial  asthma,  and  in  fibrinous  bronchitis  of 
the  smaller  tubes. 

Mechanical  restriction  of  the  thoracic  movements  provokes  dyspnea, 
commonly  of  the  mixed  type,  attended  by  accelerated  breathing, 
and  by  compensatory  overaction  of  the  unaffected  side,  in  unilateral 
interferences.  The  causes  underlying  this  variety  of  dyspnea  are 
practically  those  of  deficient  expansion  (q.  v.),  namely:  conditions 
provocative  of  painful  breathing;  rigidity  and  deformity  of  the  bony 
thorax;  intra thoracic  tumor  and  paralysis  of  the  respiratory  muscles; 
pleural  collections  of  gas  or  fluid;  and  upward  displacement  of  the 
diaphragm  by  enlarged  abdominal  viscera,  tumor,  meteorism,  or 
ascites. 

Pulmonary  Dyspnea. — Diminution  of  the  respiratory  surface, 
due  to  diseases  of  the  pulmonary  parenchyma,  is  attended  by  dysp- 
nea and  rapid  breathing,  the  degrees  of  which  are  determined  chiefly 
by  the  extent  to  which  pulmonary  ventilation  is  crippled.  In  some 
instances  the  attendant  toxemia  is  also  actively  concerned,  and  in 
others  some  of  the  additional  factors  of  dyspnea  enumerated  above 
are  partly  responsible.  Pulmonary  dyspnea  may  be  met  with  in  any 
form  of  consolidation,  collapse,  or  distention  of  the  lungs,  of  which 
good  examples  are  furnished  by  croupous  pneumonia,  tuberculosis, 
edema,  infarction,  fibrosis,  and  neoplasm;  by  atelectasis  due  to 
catarrhal  pneumonia  and  to  pericardial  or  pleural  effusion;  and  by 
the  overinflation  of  the  vesicles  in  hyperrrophic  emphysema.  In 
the  last-named  disease  a  highly  distinctive  expiratory  dyspnea  pre- 
vails; in  most  of  the  others  there  is  difficulty  with  both  inspiration 
and  expiration. 

Cardiac  Dyspnea. — The  dyspnea  of  uncompensated  cardiac  dis- 
ease depends  upon  general  circulatory  stasis,  by  fault  of  which  the 
system  is  overcharged  with  venous  blood,  the  oxygen  tension  being 
lowered  with  a  consequent  increased  stimulation  of  the  respira- 
tory center.  Owing  to  this  defect,  the  lungs  become  rigidly  fixed 
in  the  position  of  extreme  inspiration,  on  account  of  the  great 
overdistension  of  the  pulmonary  capillaries  with  blood.  These 
two  circumstances  excite  the  rapid,  shallow,  arhythrnic  dyspnea 
which  develops  in  various  structural  lesions  of  the  heart,  but 
especially  in  mitral  disease,  during  the  stage  of  broken  compensa- 


104  PHYSICAL   DIAGNOSIS 

tion.  The  associated  bronchitis,  with  its  abundant  catarrhal  secre- 
tion, aggravates  the  respiratory  distress  already  existing.  Sud- 
den, acute  engorgement  of  the  pulmonary  capillaries  gives  rise  to 
urgent  dyspnea  and  cardiac  irregularity — the  condition  mistermed 
"cardiac  asthma,"  which  is  to  be  clearly  distinguished  from  true 
bronchial  asthma  and  from  uremic  dyspnea. 

CYANOSIS 

Cyanosis  betrays  a  deficiency  of  oxygen  and  an  excess  of  carbon 
dioxid  in  the  capillary  circulation,  and  is  recognized  as  a  dusky  blue 
or  even  purple  discoloration  of  the  skin  and  the  mucous  membranes. 
This  discoloration  tends  to  show  most  decidedly  in  relatively  trans- 
parent parts  remote  from  the  chest — the  tips  of  the  fingers  and  toes, 
the  knees  and  ankles,  and  the  lips,  nose,  cheeks,  and  ears.  Cyanosis 
blended  with  pallor  gives  to  the  skin  a  livid  hue,  and  combined  with 
jaundice,  an  extraordinary  greenish  tint. 

The  factors  of  general  cyanosis  relate  to  the  faulty  oxygenation  of 
the  blood  in  the  lungs,  and  to  any  obstruction  of  the  venous  return 
flow  productive  of  congestion  within  the  veins.  Like  dyspnea, 
cyanosis  may  accompany  disorders  of  the  cardiovascular  or  respiratory 
system,  capable  of  exciting  the  foregoing  disturbances.  Aside  from 
such  causes  as  these,  cyanosis  is  symptomatic  of  vasomotor  paralysis 
and  of  the  methemoglobinemia  consequent  to  poisoning  by  acetanilid 
or  by  nitrobenzol.  Permanent  cyanosis  with  splenomegaly  and 
polycythemia  constitutes  the  syndrome  of  Saundby  and  Russell, 
chronic  cyanotic  polycythemia. 

Local  cyanosis  is  produced  by  either  partial  or  complete  oblitera- 
tion of  a  venous  trunk  by  thrombosis  or  by  external  pressure,  in 
consequence  of  which  blueness  develops  in  the  part  distal  to  the 
constriction. 

VENOUS  ENLARGEMENT  AND  TORTUOSITY 

Actual  overfulness  of  the  veins  upon  the  surface  of  the  thorax  is  to  be 
distinguished  from  the  conspicuous  venous  trunks  so  commonly 
observed  in  the  thin-skinned  blond  and  in  those  who  are  greatly 
emaciated.  In  a  healthy  person  one  occasionally  meets  with  a  general 
dilatation  and  even  with  an  abnormal  tortuosity  of  the  cutaneous 
veins  of  the  chest,  a  peculiarity  best  explained  by  ascribing  it  to  a  con- 
genital weakness  of  the  venous  walls.  More  often,  however,  venous 
enlargement  is  traceable  to  either  a  general  or  a  local  interference 
with  the  venous  circulation,  due,  for  instance,  to  right-sided  cardiac 


EXAMINATION  OF  THE  THORAX 


105 


weakness,  to  thrombosis,  and  to  mediastinal  growths  (Figs.  50  and 
51).  The  direction  of  the  venous  flow  is  determined  by  stroking  the 
enlarged  vein  so  as  to  empty  the  blood  therein,  and  then  noting  the 
direction  from  which  the  collapsed  vessel  refills  when  the  pressure 
is  removed.  Or  the  vein  may  be  compressed  with  the  finger-tip 
and  the  relation  of  the  resulting  turgescence  to  the  point  of  con- 
striction observed  (cf.  p.  5 14) . 

Enlarged  mammary  veins  may  arise  from  several  different  causes: 
they  are  not  uncommon  during  the  late  stages  of  pregnancy  and 
during  lactation;  they  are  also  associated  with  many  cases  of  malig- 
nant disease  of  the  breasts;  and  they  may  betray  an  obstruction,  by 


Fig.  50. — Venous  tortuosity  of  the  thoracic  wall  (Episcopal  Hospital). 

the  pressure  of  a  thoracic  aneurism  or  a  new-growth,  to  the  venous 
return  of  blood  from  the  breasts. 

A  ramification  of  small  venules  over  the  upper  chest,  with 
prominence  of  the  jugulars,  is  sometimes  found  in  tuberculous 
enlargement  of  the  bronchial  glands.  Abnormal  fulness  of  the 
superficial  veins  in  the  neighborhood  of  the  sternum  suggests  medias- 
tinal tumor,'  of  which  such  a  sign  is  one  of  the  early  clinical  manifesta- 
tions (Fig.  50) .  The  pressure  of  a  tumor  or  of  a  cicatrix  in  the  axilla 
may  account  for  overdistention  of  the  veins  of  the  upper  arm  on  the 


io6 


PHYSICAL   DIAGNOSIS 


affected  side  (Fig.  52).  A  purplish  fringe  of  dilated  veins  coursing 
symmetrically  along  the  costal  arch  is  a  familiar  finding  in  right  ven- 
tricular dilatation,  in  atrophic  cirrhosis  of  the  liver,  and  in  chronic 
adhesive  pleurisy.  In  portal  vein  engorgement  and  obstruction 


Fig  51. — Venous  engorgement  of  thoracic  and  abdominal  walls  (Jefferson  Hospital). 

the  greater  part  of  the  entire  lower  thorax  is  sometimes  encroached 
upon  by  the  upward  extension  of  the  dilated  veins  of  the  upper 
abdominal  region. 

EDEMA  OF  THE  THORACIC  WALL 

This  is  easily  detected  by  its  tumid  appearance  and  by  the  fact 
that  the  tissues  pit  upon  pressure  and  retain  temporarily  the  imprint  of 
the  finger.  Local  edema,  perhaps  with  some  discoloration,  may  be  a 
sign  of  impending  perforation  in  empyema  necessitatis  or  of  abscess 
of  the  parietes;  but  purulent  pericarditis,  mediastinal  abscess,  pul- 
monary hydatid,  aneurism  of  the  aortic  arch,  and  angioneurotic 
edema  must  also  be  recalled  as  possible  factors.  Occlusion  of  the 


EXAMINATION   OF    THE    THORAX 


107 


Fig.  52. — Edema  of  the  arm,  due  to  lymphatic  obstruction  (Jefferson  Hospital). 


.      > 


Fig.  53.— Edema  of  the  lower  extremities  (Jefferson  Hospital). 


io8 


PHYSICAL   DIAGNOSIS 


Fig.  54. — Nephritic  edema  of  the  face  (Jefferson  Hospital). 


Fig.   55. — Cardiorenal  anasarca  (Jefferson  Hospital). 


EXAMINATION    OF    THE    THORAX 

superior  vena  cava  may  account  for  persistent  edema  of  the  thorax, 
neck,  and  upper  limbs,  with  cyanosis  and  compensatory  dilatation 
of  the  superficial  veins.  General  edema  affecting  the  greater  part 
of  the  surface  of  the  chest,  is  referable  to  some  form  of  anasarca, 
for  the  cause  of  which  the  heart,  the  liver,  and  the  kidneys  should 
be  examined  (Fig.  55).  In  this  connection  that  form  of  congenital 
dropsy  known  as  fetal  erythroblastosis,  a  defective  hemogenesis 
with  anasarca  and  fluid  hi  the  body  cavities,  should  be  recalled. 

GLANDULAR  ENLARGEMENT 

Routine  examination  of  the  neck  and  axilla  should  be  made,  in 
order  to  detect  glandular  swellings  symptomatic  of  such  lesions  as 
simple  adenitis,  tuberculosis,  syphilis,  malignant  tumors,  benign 


••• 

Fig.  56. — Common  sites  of  superficial  glandular  enlargements. 

lymphoma,  leukemia,  and  Hodgkin's  disease.     The  cervical  glands, 
lying  along  and  beneath  the  sternocleidomastoid  muscle,  are  the 


HO  PHYSICAL   DIAGNOSIS 

favorite  site  of  simple  acute  adenitis  tending  to  end  by  resolution, 
and  met  with  in  the  specific  fevers  of  childhood  and  in  local  infec- 
tions of  neighboring  parts.  Of  the  former  class  of  factors,  measles, 
scarlatina,  diphtheria,  glandular  fever,  and  pertussis  are  important 
examples;  and  of  the  latter  group  of  causes,  dental  caries,  stomatitis, 
tonsillitis,  and  otitis.  The  submaxillary  glands  are  frequently  the 
earliest  site  of  tuberculous  adenitis,  which  in  the  course  of  time  tends 
to  implicate  the  other  lymphatics  of  the  neck  (Fig.  59).  Scrofulous 
glands  are  prone  to  early  softening,  suppuration,  and  fistulation, 
and  are  often  accompanied  by  definite  signs  of  tuberculosis  of  the 
lungs  and  bronchial  glands.  These  glands  are  also  a  favorite  site  for 


Fig.  57- — Benign  tumor  of  the  neck  (Jefferson  Hospital). 

the  growth  of  a  local  benign  lymphoma,  a  tumor  of  this  type  being 
strictly  limited  to  a  single  group  of  glands,  and  forming  a  dense, 
painless  swelling  which  does  not  caseate,  suppurate,  nor  adhere  to 
adjacent  parts  (Fig.  58).  Vincent's  angina,  diphtheria,  mumps, 
stomatitis,  actinomycosis,  and  infections  of  the  mouth  and  adjacent 
structures  are  among  the  other  factors  of  submaxillary  adenitis. 
The  occipital  glands  are  commonly  enlarged  in  syphilis,  being  recog- 
nized as  a  group  of  painless,  freely  movable  masses  of  cartilaginous 


EXAMINATION    OF    THE    THORAX 


III 


58. — Lymphoma  of  the  cervical  glands  (Jefferson  Hospital). 


Fig.     59. — Bilateral    tuberculous    enlargement    of    the    cervical    lymphatic    glands 
(Jefferson  Hospital). 


112 


PHYSICAL   DIAGNOSIS 


hardness  and  moderate  size.    Whenever  such  masses  are  felt,  the 
examiner  should  look  for  the  initial  lesion  and  search  for  inguinal 

' 


Fig.    60. — Bilateral   sarcomatous   enlargement   of   the   cervical    lymphatic   glands 
(Jefferson  Hospital). 


Fig.  6v — Generalized    glandular    enlargement    in    Hodgkin's    disease   (Jefferson 

Hospital). 

adenitis  and  for  supratrochlear  kernels  just  above  the  internal 
condyle  of  the  humerus.    The  posterior  cervical,  glands  are  pecu- 


EXAMINATION   OF    THE    THORAX  113 

liarly  susceptible  to  enlargement  in  rotheln,  and  the  occipital 
glands  are  affected  in  irritation  and  inflammation  of  the  scalp. 
Enlargement  of  the  parotid  gland,  aside  from  mumps  and  neo- 
plasms, may  be  secondary  to  septicemia,  pneumonia,  enteric  fever, 
and  similar  infections;  to  lesions  of  the  abdomen  and  pelvis;  and 
to  facial  paralysis. 


Fig.  62. — Cystic  enlargement  of  the  thyroid  gland  (Jefferson  Hospital). 

Enlargements  of  the  axillary  glands  (Fig.  61)  may  be  secondary 
to  vaccinia,  infected  wounds,  general  septicemia,  and  bubonic 
plague;  they  are  part  and  parcel  of  the  general  glandular  hyper- 
plasia  of  Hodgkin's  disease  and  of  leukemia;  and,  like  many  of 
the  lymphatic  chains  heretofore  mentioned,  they  are  sometimes 
symptomatic  of  malignant  tumors.  The  extensive  glandular  tu- 
mors of  Hodgkin's  disease  and  of  leukemia  are  in  nowise  dis- 
tinctive, from  a  clinical  standpoint,  but  the  blood-report  furnishes 
an  easy  means  of  differentiation :  normal  or  but  moderately  anemic 
blood  in  the  former,  and  either  myelemia  or  lymphemia  in  the 
latter.  A  malignant  neoplasm  of  the  lymphatic  structures,  if 


PHYSICAL   DIAGNOSIS 


cancerous,  is  to  be  regarded  as  secondary  to  a  primary  growth 
in  another  situation — in  the  mouth,  the  upper  air-passages,  or 
the  mediastinum,  if  the  cervical  lymphatics  are  implicated;  in 
the  breast,  if  the  axillary  glands  are  large.  A  sarcomatous  gland- 


Fig.  63. — Subcutaneous  nodules  in  a  case  of  general  sarcomatosis  (Jefferson  Hospital). 

ular  swelling  is  likely  to  be  fixed  and  immovable,  and  tends  early 
to  infiltrate,  inflame,  and  ulcerate  adjacent  tissues.  The  soft  parts 
about  a  lymphosarcoma  may  pit  upon  pressure,  if,  indeed,  they 
do  not  seem  abscessed,  and  the  tumor  is  sometimes  covered  by  a 
maze  of  tortuous,  congested  cutaneous  veins. 

Enlargement  of  the  lateral  thoracic  glands  in  the  midaxilla  is 
suggestive  of  tuberculosis,  either  pulmonary  or  bronchial.  Zeb- 
rowski  found  this  type  of  adenitis  hi  20  per  cent,  of  all  cases  of 
phthisis,  usually  on  the  side  of  the  affected  lung.  Other  factors 
of  enlarged  glands  in  this  site  include  simple  hyperplasia,  malig- 
nant neoplasms  of  the  lung,  pleura,  mediastinum,  liver  and  stom- 
ach, lymphatic  leukemia,  and  Hanot's  hepatic  cirrhosis. 


Fig.  64. — Thyroid  enlargement  in  Graves'  disease  (Jefferson  Hospital). 


Fig.  65. — Thyroid  enlargement  in  Graves'  disease  (without  exoohthalmos)  .(Jefferson 

Hospital). 


n6 


PHYSICAL   DIAGNOSIS 


Enlargement  of  the  thyroid  gland  shows  as  a  globular  swelling, 
more  often  of  irregular  than  of  symmetric  contour,  situated  between 
the  larynx  and  the  suprasternal  notch,  and  intimately  attached  to 
the  trachea,  with  which  it  moves  during  deglutition  (Fig.  62).  Such 
a  tumor  generally  proves  to  be  goitrous,  either  simple  cystic  or  exoph- 
thalmic, the  ordinary  bronchocele  being  attended  by  no  ill  effects 
save  perhaps  those  due  to  pressure,,  while  in  Graves'  disease  one 
expects  to  find  three  other  cardinal  signs — tachycardia,  exophthalmos, 


Fig.  66.— Multiple  fibroma  (molluscum  fibrosum)  of  the  back  (Philadelphia  General 

Hospital). 

and  tremor  (Figs.  64  and  65).  Less  commonly  the  enlargement  is 
due  to  acute  thyroiditis,  abscess,  tuberculosis,  neoplasm,  or  acro- 
megaly.  Puberty  in  girls,  menstruation,  and  pregnancy  all  may 
be  accompanied  by  a  moderate,  transient  swelling  of  the  thyroid 


EXAMINATION    OF    THE    THORAX  117 

gland,  excited  by  acute  congestion.  Myxedema,  in  the  form  of 
either  cretinism  or  Gull's  disease,  is  characterized  by  atrophy  of  the 
thyroid,  and  this  also  is  true  of  the  exceptional  case  of  acromegaly. 

PAIN   IN   THE  THORAX 

Pain  in  the  chest  may  be  symptomatic  not  only  of  diseases  of  the 
thorax  and  its  contents,  but  also  of  lesions  affecting  more  remote 
regions,  such  as  the  gastro-intestinal  and  the  genito-urinary  tracts, 
the  peritoneum,  the  spine,  and  other  parts  of  the  nervous  system. 
Such  extrathoracic  factors  as  these  are  to  be  recalled  in  deciding 
the  origin  of  pains  affecting  the  thorax.  Of  the  many  localized  chest 
pains,  those  referred  to  the  apex  of  the  lung,  the  sternum,  the  breast, 
the  precordia,  the  back,  and  the  lower  thoracic  regions  have,  in  many 
instances,  more  or  less  definite  significance;  but,  as  a  rule,  the  various 
unclassified  pains  felt  in  other  areas  of  the  chest  are  most  ambiguous 
clues  (Fig.  67). 

Pain  in  the  right  shoulder  is  occasionally  an  accompaniment  of 
aortitis  and  of  aneurism  of  the  innominate  artery,  but  more  often 
it  is  due  to  some  disease  of  the  liver  or  of  the  bile-ducts.  Possible 
factors  of  pain  in  the  left  shoulder  include  diaphragmatic  pleurisy, 
distention  of  the  colon,  gastritis,  gastrectasis,  duodenal  ulcer,  and 
suprarenal  lesions. 

At  the  apex  of  the  lung  pain  is  commonly  elicited  in  apical  tuber- 
culosis, owing  to  the  attendant  pleurisy. 

Sternal  pain  may  mean  bronchitis,  enlarged  bronchial  glands,  or 
bronchial  obstruction  by  a  foreign  body;  aortitis,  aortic  valvulitis, 
aortic  aneurism,  or  angina  pectoris;  and  mediastinal  inflammation, 
abscess,  or  tumor.  Pain  in  this  situation  is  also  very  common  in 
gastric  disorders,  in  syphilis,  and  in  diseases  of  the  bone  itself. 

Pain  in  the  precordia,  which  is  quite  as  likely  to  be  extracardiac 
as  cardiac,  has  among  its  numerous  factors  functional  and  organic 
cardiac  disease,  aneurism  of  the  aorta,  angina  pectoris,  neuralgia, 
myalgia,  and  disorders  of  the  stomach  and  the  colon. 

Pain  in  the  breast,  aside  from  that  due  to  diseases  of  the  mammae, 
may  be  associated  with  menstruation,  pregnancy,  and  lesions  of  the 
uterus  and  the  ovaries.  Pleural  pains,  as  in  the  pleurisy  of  croupous 
pneumonia,  are  also  ordinarily  referred  to  this  region. 

Pain  in  the  right  hypochondrium  suggests  especially  diseases  of  the 
liver  and  the  bile-passages,  malignant  growths  of  the  pancreas,  the 
hepatic  colon,  or  the  duodenum,  and  aortic  valve  defects;  in  the 
left  hypochondrium,  pain  may  be  due  to  diseases  of  the  spleen, 
impaction  of  the  splenic  colon,  inflammation,  ulceration,  dilatation 


n8 


PHYSICAL    DIAGNOSIS 


and  prolapse  of  the  stomach,  and  aneurism  of  the  abdominal 
aorta.  As  likely  causes  of  pain  in  either  hypochondrium  pleurisy, 
pneumonia,  subphrenic  abscess,  peritonitis,  gastric  cancer,  renal 


1 


m  i 
*li  m 

•gif  «ji  f-il 

g||  g  .2  fc.S  ( 

ill*  ' 


kai 


•a^  1-i-eJ 


if-|  -^.  p-«a>rf-=5 

f!  !! 

<  K       Q  S 

colic,  and  nephroptosis  are  to  be  recalled.  Pain  localized  along 
the  upper  part  of  the  costal  arch  may  be  symptomatic  of  dia- 
phragmatic pleurisy,  or  it  may  come  from  the  strain  of  long- 
continued  coughing  or  retching. 


EXAMINATION    OF    THE    THORAX 


Pain  in  the  lateral  wall  of  the  thorax  is  particularly  significant  of 
pleurisy,  pleurodynia,  and  intercostal  neuralgia,  and  in  this  region 
may  also  be  felt  the  pain  of  pericarditis,  thoracic  aneurism,  mediastinal 
disease,  and  lesions  of  the  vertebrae.  Herpes  zoster  accounts  for 
exquisite  pain  in  the  lateral  thorax,  especially  on  the  right  side.  The 
discomfort  attending  gaseous  distention  of  the  stomach  and  colon, 
as  well  as  that  of  fecal  impaction  of  the  colon,  is  also  referred  to  the 
side  of  the  chest  in  many  instances.  Indefinite  pains  in  the  side  are 
a  common  complaint  in  hysteric  and  in  anemic  states. 

Pain  in  the  posterior  thoracic  wall  (Fig.  68) .  if  localized  between  the 


Arterial  hypertension ; 
constipation ;  gastric 
lesions. 


Gastric  ulcer. 


Splenitis  ;   pancreatitis. 


Pericarditis ;          phrenic 
pleurisy. 


Hepatic  disease. 


Thoracic  aneurism  ;  me- 
diastinal disease ;  gas- 
tro-intestinal,  esopha- 
geal,  and  pancreatic 
lesions. 

Colonic  lesions. 

Renal  disease. 

.  Pleurisy ;      appendicitis ; 

abdominal     neoplasm ; 

lumbago. 

'  Pelvic  disease ;  sacro- 
i  iliac  and  hip-joint  dis- 
•  ease  ;  rectal  lesions. 


Fig.  68. — Areas  of  dorsal  tenderness  and  pain. 

scapulae  at  the  level  of  their  spines,  may  mean  either  pericarditis  or 
diaphragmatic  pleurisy;  at  the  inferior  angle  of  the  left  scapula,  spleni- 
tis;  and  at  the  inferior  angle  of  the  right  scapula,  disease  of  the  liver. 
In  phthisis  an  interlobar  pleurisy  commonly  provokes  a  dull  ache, 
changed  by  coughing  to  a  sharp,  lancinating  pain  alongside  the  spine, 
at  the  level  of  the  second  or  third  thoracic  vertebra,  or  the  point  cor- 
responding to  the  inner  border  of  the  oblique  fissure  between  the 
upper  and  lower  pulmonary  lobes.  Pain  between  the  scapulae  is 


120 


PHYSICAL   DIAGNOSIS 


frequently  due  to  some  disorder  of  the  stomach,  such  as  overdisten- 
tion,  inflammation,  or  ulceration;  tenderness  at  the  left  of  the  spine 
at  the  level  of  the  eleventh  and  twelfth  thoracic  vertebrae  is  frequently 
elicited  in  gastric  ulcer.  The  gnawing  pain  of  an  aneurism  of  the 
descending  aorta  is  felt  between  the  left  scapula  and  the  spinal 
column. 

Here  also  may  be  mentioned  the  principal  factors  of  pain  in  the 
loin  and  in  the  sacral  region.  Aching  and  pain  in  the  lumbar  region, 
usually  radiating  to  the  flanks,  constitute  a  familiar  symptom  in 
lumbago,  lumbar  neuralgia,  dysmenorrhea,  lithemia,  and  in  con- 


Fig.  69. — Empyema  necessitatis  (Jefferson  Hospital). 

ditions  of  simple  exhaustion  and  neurasthenia;  it  may  be  a  sign  of  a 
more  grave  disorder — renal  lesions,  lumbar  abscess,  appendicitis, 
hernia,  and  abdominal  aneurism  or  neoplasm;  or  it  may  be  referred 
to  diseases  of  the  bladder,  the  prostate,  the  perineum,  and  the  rectum. 
The  lumbar  region  is  the  favorite  seat  of  the  dragging  ache  excited 
by  a  mass  of  feces  within  the  colon,  and  of  the  pain  which  attends 
many  of  the  acute  febrile  infections. 

Pain  in  the  region  of  the  sacrum  is  a  finding  which  points  perti- 
nently to  diseases  of  the  pelvis  and  its  viscera,  and  one  which  also 
suggests  sciatica,  sacral  neuralgia,  sacro-iliac  disease,  coxalgia, 
inflammation,  ulcer,  cancer  of  the  rectum,  and  diseases  of  the  testes. 


EXAMINATION   OF    THE    THORAX  121 

Of  the  foregoing,  sciataca  and  lesions  of  the  pelvis  and  the  rectum 
also  reflect  pain  to  the  outer  and  posterior  aspects  of  the  thigh.  In 
the  coccygeal  region  pain  is  attributable  to  such  factors  as  coccygo- 
dynia,  hemorrhoids,  proctitis,  and  fissure  or  fistula  of  the  rectum. 

Scars. — Scarring  of  the  chest-wall  and  of  the  neck  is  to  be  carefully 
investigated,  for  such  marks  are  sometimes  a  valuable  clue  in  identify- 
ing questionable  cases  of  syphilis  and  of  tuberculosis.  The  cicatrix 
left  by  a  healed  perforative  empyema,  by  a  rib  resection,  by  a  trauma, 
or  by  a  burn  may  also  throw  light  upon  the  patient's  condition.  The 
pitting  of  variola  and  of  varicella,  the  tough,  thick,  flat  scars  of  lupus, 
and  the  minute  depressions  of  acne  are  also  rather  distinctive. 

Other  signs,  noted  on  inspection  of  the  cutaneous  surface  in  general, 
rather  than  that  of  the  thorax  in  particular,  relate  to  the  temperature 
and  moisture  of  the  skin,  to  deviations  from  its  normal  color,  such 
as  pallor,  flushing,  undue  redness,  jaundice,  and  pigmentation,  and 
to  the  presence  of  petechiae,  ecchymoses,  and  various  eruptions. 

Clubbed  or  Drumstick  Fingers. — Extreme  incurving  of  the  nails, 
thickening  of  the  joints,  and  bulbous  enlargement  of  the  tips  of  the 
terminal  phalanges  are  the  hall-marks  of  this  deformity,  observed 
in  various  chronic  diseases  of  the  heart  and  the  bronchopulmonary 
system,  and  in  conditions  of  habitual  cyanosis.  Phthisis,  bron- 
chiectasis,  empyema,  chronic  adhesive  pleurisy,  pulmonary  stenosis, 
and  cardiac  septal  defects  are  prominent  factors  of  drumstick  fin- 
gers, which,  with  less  frequency,  also  occur  in  rickets,  hepatic  cirrho- 
sis, gastrectasis,  and  myxedema.  Clubbing  of  the  fingers,  with 
bilateral  enlargement  of  the  hands,  feet,  and  long  bones,  is  distinctive 
of  Marie's  hypertrophic  pulmonary  osteo-arthropathy,  a  form  of 
toxic  osteoperiostitis  incident  to  various  purulent  lesions  of  the 
bronchi,  lungs,  and  pleura. 


SECTION    III 

EXAMINATION  OF  THE  BRONCHOPULMONARY 

SYSTEM 


CLINICAL  ANATOMY 

The  Lungs. — The  lungs  are  a  pair  of  roughly  pyramidal  organs, 
closely  approximated  to  the  walls  of  the  pleural  cavity,  their  bluntly 
convex  apices  occupying  the  pleural  domes,  and  their  broad,  concave 


Fig.  70. — Radiograph  of  the  normal  thorax.     (Plate  by  Dr.  W.  F.  Manges.) 

bases  resting  upon  the  diaphragm.     Of  the  two  lungs,  the  left  is 
somewhat  longer,  narrower,  and  less  voluminous  than  the  right. 

The  outer  or  costal  surfaces  of  the  lungs,  which  are  convex,  are  closely 
adapted  to  the  inner  pleural  surfaces  of  the  ribs  and  the  intercostal 
spaces.  The  inner  or  mediastinal  surfaces  bound  the  mediastinum 


EXAMINATION   OF   THE   BRONCHOPULMONARY    SYSTEM 


123 


and  are  deeply  indented,  especially  on  the  left  side,  to  afford  room 
for  the  heart.  Above  and  behind  this  hollow  space  is  the  wedge- 
shaped  hilus  of  the  lung,  within  which  the  bronchi,  the  pulmonary 
artery,  pulmonary  veins  and  nerves,  the  bronchial  vessels,  and  the 
lymphatics  communicate  with  the  lungs.  These  structures,  entering 
and  leaving  at  the  hilus,  constitute  the  root  of  the  lung,  which  lies 
opposite  the  fourth,  fifth,  and  sixth  thoracic  vertebrae.  The  inner 
pulmonary  surfaces  are  grooved  on  the  right  side  for  the  superior  vena 


Fig.  71- — Anterior  surface  topography  of  the  lungs,  bronchi,  and  pleurae. 

cava,  the  vena  azygos  major,  and  the  innominate  vessels;  and  on  the 
left  side  for  the  aorta,  the  subclavian  artery,  and  the  innominate 
vein.  Anchored  only  by  its  root  and  ligamentum  latum  pulmonis, 
each  lung  is  otherwise  unattached  to  its  pleural  space,  in  which, 
therefore,  it  has  unhampered  motility. 

The  apices  of  the  lungs  rise  from  \  to  ij  inches  (1.25  to  3.75  cm.) 
above  the  clavicles,  the  right  apex  being  about  \  inch  (1.25  cm.)  higher 
than  the  left.  From  the  apex  the  anterior  border  of  the  right  lung 


124 


PHYSICAL   DIAGNOSIS 


is  traced  by  a  line  running  through  the  sternoclavicular  articulation 
to  the  midsternal  line,  at  the  level  of  the  second  chondrosternal  joint, 
from  which  point  it  drops  vertically  downward  to  the  level  of  the  sixth 
costal  cartilage.  The  anterior  border  of  the  left  lung  corresponds  to 
that  of  the  right  as  far  down  as  the  fourth  costal  cartilage,  but  at  this 
level  it  curves  outward  along  the  lower  border  of  the  fourth  rib  as 
far  as  the  parasternal  line,  then  drops  vertically  downward  to  the 
upper  border  of  the  fifth  rib,  and  courses  inward  to  a  point  upon  the 


Fig.    72-— Posterior  surface  topography  of  lungs,  bronchi,  and  pleura:. 

upper  border  of  the  sixth  costal  cartilage,  just  inside  the  parasternal 
line.  This  notched  contour  of  the  left  anterior  pulmonary  margin 
overlies  the  right  ventricle,  which,  uncovered  by  lung  tissue,  corre- 
sponds to  the  area  of  superficial  cardiac  dulness,  or  cardiac  flatness. 

The  lower  borders  of  the  lungs  are  represented  by  a  line  running 
outward  from  each  lower  extremity  of  the  anterior  border,  and,  coin- 
ciding with  the  sixth  rib  in  the  midclavicular  line,  the  eighth  rib  in 
the  midaxillary  line,  the  tenth  rib  in  the  scapular  line,  and  the  tenth 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM 


125 


thoracic  vertebra  in  the  midspinal  line.  Since  the  inferior  margin  of 
the  right  and  the  left  lung  may  be  considered  identical  clinically,  the 
foregoing  surface-marking  applies  to  each. 

The  three  lobes  of  the  right  lung  are  indicated  by  the  courses  of 
its  oblique  and  horizontal  fissures,  while  the  two  lobes  of  the  left 
lung  are  separated  by  its  single  fissure,  the  oblique.  The  position 
of  the  oblique  fissures,  which  is  the  same  in  each  lung,  is  marked  by 


\ 


Fig.  73 — Right  lateral  surface  topog- 
raphy of  the  lungs  and  pleurae. 


Fig.  74.— Left  lateral  surface  topog- 
raphy of  the  lungs  and  pleurae. 


a  line  beginning  at  the  second  thoracic  spinous  process,  continuing 
downward  and  forward  through  the  root  of  the  scapular  spine  to  the 
fourth  rib  in  the  midaxillary  line,  and  terminating  at  the  lower  border 
of  the  lung  at  the  sixth  costal  cartilage,  just  inside  the  parasternal  line. 
The  line  of  the  horizontal  fissure  of  the  right  lung  begins  at  the  anterior 
pulmonary  border  at  the  level  of  the  fourth  costal  cartilage,  and 
extends  outward  below  the  fourth  rib  as  far  as  the  midaxillary  line, 
where  it  joins  the  oblique  fissure. 


I26  PHYSICAL    DIAGNOSIS 

Making  use  of  these  interlobar  landmarks,  the  following  limits  of 
the  pulmonary  lobes  can  be  mapped  out  upon  the  surface  of  the 
body:  The  riglit  anterior  thorax  overlies  the  upper  lobe  from  the 
supraclavicular  space  to  the  fourth  rib;  the  middle  lobe,  from  the 
fourth  to  the  sixth  ribs;  and  a  triangular  portion  of  the  lower  lobe, 
below  and  outside  the  latter  level.  Upon  the  left  anterior  thorax 
the  upper  lobe  extends  downward  as  far  as  the  junction  of  the  sixth 
costal  cartilage  and  the  lower  pulmonary  border,  below  which  level 
the  lower  lobe  extends  to  the  left.  Upon  the  right  lateral  thorax 
the  point  at  which  the  midaxillary  line  crosses  the  fourth  rib  marks 
the  junction  of  the  upper,  the  middle,  and  the  lower  lobes.  The 
same  point  upon  the  left  lateral  thorax  divides  the  upper  and  the 
lower  lobes  of  the  left  lung.  Upon  the  posterior  thorax  on  each  side 
the  greater  part  of  the  upper  lobe  lies  above  the  scapular  spine,  below 
which  is  the  lower  lobe,  extending  downward  to  the  level  of  the  tenth 
thoracic  vertebra. 

The  Bronchi  and  Trachea. — The  trachea  begins  at  the  lower 
border  of  the  cricoid  cartilage,  enters  the  mediastinal  space  at  the 
level  of  the  seventh  cervical  vertebra,  and  terminates  by  division  into 
the  right  and  left  primary  bronchial  tubes,  at  the  level  of  the  root 
of  the  scapular  spine  posteriorly,  or  at  the  angle  of  Louis  anteriorly. 
The  bronchi  extend  obliquely  downward  and  outward  from  the 
bifurcation  of  the  trachea  to  the  root  of  each  lung,  the  right  bronchus 
entering  the  corresponding  lung  at  a  somewhat  higher  level  than  the 
left.  The  right  bronchus  differs  from  the  left  in  being  shorter,  of 
larger  diameter,  and  of  more  vertical  course — hence  the  relatively 
exaggerated  physical  signs  over  this  tube,  as  well  as  its  greater  pre- 
dilection for  foreign  bodies  that  pass  below  the  division  of  the  wind- 
pipe. The  bronchial  lymphatic  glands,  which  are  especially  numer- 
ous near  the  tracheobronchial  junction,  extend  along  each  bronchial 
tube  toward  the  root  of  the  lung.  These  glands,  when  tuberculous 
or  otherwise  diseased,  may,  by  pressure,  inflammation,  and  infec- 
tion, seriously  implicate  the  bronchi,  the  trachea,  the  esophagus, 
and  the  pericardium. 

The  Pleurae. — The  pleural  cavities,  which  contain  the  lungs,  are 
lined  each  with  a  separate  pleural  membrane,  one  layer  being  in 
intimate  relation  with  the  thoracic  parietes  (parietal  pleura),  and  a 
second  layer  closely  investing  the  lungs  (visceral  pleura).  The 
parietal  pleura,  though  a  continuous  membrane,  is  arbitrarily  divided 
into  several  parts  (cervical,  costal,  diaphragmatic,  mediastinal), 
corresponding  to  different  areas  of  the  thoracic  chamber.  The  sig- 
nificance of  these  artificial  divisions  of  the  pleural  covering  is  self- 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM      127 

evident.  The  -visceral  pleura  closely  adheres  to  the  lung,  both  upon 
its  external  and  interlobar  surfaces,  and  at  the  pulmonary  root  it 
becomes  continuous  with  the  mediastinal  part  of  the  parietal  pleura. 

The  surface  line  of  the  right  pleura  extends  anteriorly  from  the 
sternoclavicular  articulation  to  the  level  of  the  second  chondrosternal 
joint  at  the  left  of  the  midsternal  line,  whence  it  continues  downward 
to  the  ensiform  process,  and  then  is  deflected  to  the  right,  crossing 
the  lower  border  of  the  seventh  rib  in  the  midclavicular  line,  the  tenth 
rib  in  the  midaxillary  line,  and  the  upper  border  of  the  twelfth  thoracic 
vertebra  at  the  spine.  The  line  of  the  left  pleura  descends  from  the 
left  sternoclavicular  joint  parallel  to  the  course  of  the  right  pleura, 
running  beneath  the  outer  third  of  the  sternum  as  far  as  the  fourth 
rib;  at  this  level,  however,  it  turns  obliquely  to  the  left  sternal  edge, 
beneath  which  it  resumes  a  vertically  downward  course  to  a  point 
in  the  middle  of  the  sixth  costal  cartilage;  thence  the  line  follows, 
at  a  somewhat  lower  level,  the  same  course  as  the  pleural  line  of  the 
right  side  to  the  vertebral  column.  Posteriorly,  both  pleurae  parallel 
the  spine  from  the  first  to  the  twelfth  thoracic  vertebra. 

The  space  lying  between  the  two  pleurae  beneath  the  sternum 
corresponds  to  the  situation  of  the  anterior  mediastinum.  The 
apex  of  the  pleural  cavity,  inclosing  the  pulmonary  apex,  is  bounded 
by  a  pyramidal  line  running  from  the  sternoclavicular  joint  to  meet 
the  posterior  pleural  border  at  the  level  of  the  first  thoracic  vertebra 
posteriorly.  The  slight  outward  deviation  of  the  left  anterior  pleural 
line  below  the  fourth  rib  exposes  the  pericardium  to  immediate  con- 
tact with  the  sternum.  The  recess  intervening  between  the  lower 
pulmonary  and  pleural  borders  is  known  as  the  complementary 
pleural  space;  this  sinus,  largely  occupied  by  the  lungs  when  they  are 
fully  inflated,  during  their  deflation  varies  in  depth  from  i\  to  3$ 
inches  (3.75  to  8.75  cm.),  being  deepest  on  the  lateral  chest-wall,  and 
extends  vertically  from  about  the  sixth  to  the  seventh  rib  in  the 
midclavicular  line,  from  the  eighth  or  ninth  to  the  tenth  rib  in  the 
midaxillary  line,  and  from  the  tenth  to  the  twelfth  thoracic  vertebra 
in  the  midspinal  line. 

The  Mediastinum. — The  intrapleural  space,  extending  from  the 
sternum  to  the  spine,  and  partitioning  the  cavity  of  the  chest 
into  two  lateral  compartments  inclosing  the  lungs  and  pleurae,  is 
termed  the  mediastinum  thoracis,  or  the  mediastinal  space.  The 
pleural  surfaces  surrounding  this  space  are  continuous  with  the  costal 
pleurae  above  the  superior  outlet  of  the  thorax,  while  at  its  base  the 
mediastinum  is  attached  to  the  diaphragm.  The  important  structures 
inclosed  by  the  mediastinum  include  the  heart  and  its  great  vascular 


128  PHYSICAL    DIAGNOSIS 

trunks,  the  trachea,  esophagus,  and  thoracic  duct,  the  thymus  gland 
or  its  remnants,  the  bronchial  and  mediastinal  glands,  and  the  pneu- 
mogastric  and  phrenic  nerves.  It  is  convenient,  for  the  sake  of 
clear  description,  to  divide  the  mediastinum  into  four  arbitrary 
spaces, — superior,  middle,  anterior,  and  posterior, — upon  whose 
anatomic  differences  the  interpretation  of  mediastinal  physical  signs 
is  to  be  based. 

The  superior  mediastinum  lies  above  the  pericardium,  and  is 
bounded  anteriorly  by  the  manubrium  sterni,  posteriorly  by  the 
bodies  of  the  first  four  thoracic  vertebrae,  inferiorly  by  a  line  drawn 
obliquely  from  the  lower  border  of  the  fourth  thoracic  vertebra  to  that 
of  the  manubrium,  and  laterally  by  the  mediastinal  pleurae.  This 
section  of  the  mediastinum  contains  the  aortic  arch,  and  the  innomi- 
nate, left  common  carotid,  and  left  subclavian  arteries;  the  upper 
part  of  the  superior  vena  cava  and  the  innominate  veins;  the  trachea, 
esophagus,  and  thoracic  duct;  the  remains  of  the  thymus  gland  and 
the  superior  mediastinal  glands;  and  the  phrenic,  pneumogastric, 
left  recurrent  laryngeal,  and  cardiac  nerves. 

The  middle  mediastinum  comprises  the  enlarged  central  portion 
corresponding  to  the  pericardium  and  heart,  in  addition  to  which  this 
space  also  contains  the  ascending  aorta  and  its  branches,  the  pul- 
monary artery,  the  lower  part  of  the  superior  vena  cava  and  the  vena 
azygos  major,  the  bronchial  lymphatic  glands,  and  the  phrenic  nerves 
with  their  accompanying  vessels. 

The  anterior  mediastinum  is  a  triangularly  shaped  space  between 
the  sternum  and  the  pericardium,  extending  vertically  from  the  lower 
border  of  the  manubrium  to  the  sixth  or  seventh  costal  cartilages. 
It  incloses  merely  a  group  of  lymphatic  glands,  the  anterior  medias- 
tinal, embedded  in  areolar  tissue. 

The  posterior  mediastinum,  which  is  virtually  a  downward  exten- 
sion of  the  superior  space,  lies  between  the  posterior  surface  of  the 
pericardium  and  the  spine,  and  corresponds  to  the  bodies  of  the  eight 
lower  thoracic  vertebrae.  The  contents  of  this  space  are  the  de- 
scending thoracic  aorta,  the  azygos  veins,  the  esophagus,  the 
thoracic  duct,  the  pneumogastric  nerves,  and  the  posterior  medias- 
tinal lymphatic  glands. 

INSPECTION 

Inspection  bears  importantly  upon  the  diagnosis  of  pulmonary 
diseases,  the  evidences  of  which  are  in  some  instances  clearly  shown 
by  anomalies  in  the  configuration  of  the  chest  and  in  the  character 
of  its  respiratory  movements.  Cyanosis,  edema,  lymphadenitis, 
and  enlargement  of  the  superficial  veins  are  additional  signs,  often- 


EXAMINATION   OF   THE   BRONCHOPULMONARY   SYSTEM     129 

times  secondary  to  lesions  of  the  lungs.  These  physical  signs  have 
been  dealt  with  in  the  preceding  section  (p.  104  etseq.),  and,  there- 
fore, require  no  further  mention  here. 

The  examiner  should  investigate  the  thorax  systematically  from 
every  point  of  view — from  the  front,  from  the  sides,  from  behind, 
and  from  above  downward,  standing  behind  the  patient  and  looking 
down  over  the  clavicles.  The  patient,  preferably  stripped  to  the 
waist,  is  placed  in  such  a  position  that  the  light  falls  directly  upon 
the  surface  to  be  examined,  save  when  some  inconspicuous  sign,  such 
as  a  small  patch  of  deficient  expansion  or  an  ill-defined  pulsation, 
is  sought  for,  in  which  event  oblique  illumination  is  better.  The 
importance  of  routine  inspection  of  the  chest  cannot  be  insisted  upon 
too  emphatically  in  every  case  in  which  there  is  reason  to  suspect  a 
pulmonary  disorder. 

The  respiratory  turgescence  of  the  cervical  veins  is  sometimes 
an  aid  in  the  diagnosis  of  infiltrations  and  new-growths  of  the  anterior 
mediastinum.  Normally,  forcible  expiration  with  the  mouth  and 
the  nares  closed  (Valsalva's  method)  dilates  these  vessels  equally 
on  either  side,  but  should  the  intrathoracic  venous  trunks  be  com- 
pressed, the  cervical  veins  on  the  affected  side  dilate  sooner  and 
more  conspicuously  than  those  on  the  Opposite  side  of  the  neck. 

The  pressure  of  a  mass  of  enlarged  bronchial  glands  may  cause 
venous  suffusion  of  the  neck  when  the  patient's  head  is  forced  far 
backward  in  the  median  line,  thereby  exerting  upon  the  air-tubes 
sufficient  traction  to  force  the  glandular  tumor  against  the  cervical 
vessels. 

Circumscribed  areas  of  pulsation,  aside  from  those  of  precordial 
origin,  elsewhere  described  (p.  321),  are  met  with  in  certain  diseases 
of  the  lungs  and  pleura.  Pulsating  pleurisy,  usually  of  the  purulent 
type,  may  account  for  a  throbbing  or  an  undulation  in  one  or  more 
interspaces,  almost  invariably  on  the  left  side,  between  the  second 
and  the  sixth  ribs.  An  intrathoracic  pulsating  neoplasm,  by  encroach- 
ing upon  the  inner  chest-wall,  may  also  produce  a  rhythmic  surface 
throb.  A  large  cavity  of  the  left  lung,  which  abuts  directly  against 
the  heart,  may,  by  conduction  of  the  cardiac  impulse,  account  for  a 
systolic  throbbing  over  the  lower  lobe  posteriorly  (Steven). 

Displacement  of  the  larynx,  recognized  by  deviation  of  the 
pomum  Adami  from  its  median  position,  occurs  in  consequence  of 
intrathoracic  lesions  that  either  drag  or  push  the  trachea  from  its 
normal  course.  Extensive  pleural  effusion,  pneumothorax,  thoracic 
aneurism,  mediastinal  neoplasm,  pulmonary  excavation,  and  even 
a  circumscribed  dilatation  of  the  aortic  arch  are  to  be  thought  of 
as  possible  factors  of  this  deformity.  Displacement  of  the  larynx 


130  PHYSICAL   DIAGNOSIS 

by  an  adjacent  growth  ( i.  e.,  a  thyroid  tumor)  is  readily  distinguished 
from  that  due  to  the  conditions  just  noted. 

Inequality  in  the  size  of  the  pupils  is  a  pertinent  sign  in  certain 
diseases  of  the  lungs  and  pleura,  as  in  unilateral  phthisis,  pleurisy, 
and  other  lesions  exciting  irritation  of  the  sympathetic  nerve, 
as  shown  by  a  relatively  wider  pupil  on  the  affected  side.  Grober 
emphasizes  the  significance  of  deviations  from  the  normal  expiratory 
contraction  and  inspiratory  dilatation  of  the  pupils.  With  Valsalva's 
method  of  breathing  the  dilatation  of  one  pupil  with  expiration 
(bilateral  contraction  being  normal)  suggests  a  circumscribed  lesion 
on  the  same  side;  while  if  both  pupils  dilate  (instead  of  contracting), 
bilateral  disease  is  to  be  inferred — inferred,  but  not  assumed,  for 
the  value  of  these  pupillary  signs  is  to  be  decided  only  in  the  light  of 
a  full  clinical  inquiry.  The  absence  of  such  changes  by  no  means 
warrants  the  exclusion  of  thoracic  disease. 

PALPATION 

In  examining  the  lungs  the  sense  of  touch  is  used  chiefly  to 
study  various  sorts  of  fremitus,  or  vibrations  felt  over  the  pulmonary 
structure,  the  pleurae,  and  the  bronchi  when  the  subject  speaks, 
breathes,  or  coughs,  as  the  case  may  be.  In  addition,  palpation  not 
only  confirms  the  signs  afforded  by  inspection,  but  in  many  instances 
it  proves  even  more  definite,  as,  for  example,  in  recognizing  defi- 
ciencies of  expansion  and  local  asymmetry  so  slight  as  to  be  overlooked 
by  the  eye.  Different  chest  pains  and  areas  of  circumscribed  tender- 
ness— pleural,  neuralgic,  muscular — are  traced  to  their  proper 
sources  by  palpation  with  much  greater  surety  than  when  the  patient's 
statement  alone  is  relied  upon.  Tracheal  tugging,  to  be  described 
subsequently,  is  occasionally  detected  when  adhesions  exist  between 
the  trachea  or  the  large  bronchi  and  a  neoplasm  of  the  mediastinum, 
though  more  commonly  this  sign  is  symptomatic  of  aneurism  of  the 
aortic  arch  (q.  v.) . 

In  performing  palpation  the  hands  should  be  applied,  palms 
downward,  to  the  naked  skin,  and  moved  from  place  to  place  method- 
ically, so  as  to  cover  the  entire  surface  of  the  thorax,  care  being  taken 
to  compare  the  differences  of  the  two  sides,  especially  at  the  apices 
and  at  the  bases.  Aimless,  wandering  palpation  is  worse  than  none 
at  all,  and  unless  the  examination  be  systematic  and  comparative, 
the  results  will  be  misleading  and  confusing.  Lagging  respiratory 
movements  at  the  apex  are  readily  appreciated  if  the  examiner  stands 
behind  the  patient  with  his  index-  and  middle  fingers  applied  to  the 
supraclavicular  and  infraclavicular  spaces,  respectively  (Fig.  75) 


t  EXAMINATION  OF   THE   BRONCHOPULMONARY   SYSTEM     131 

Deficient  expansion  at  the  bases  is  best  determined  by  facing  the 
patient  with  the  hands  closely  pressed  against  the  curve  of  the  lower 
dorsolateral  regions  of  the  chest.  To  gage  the  general  chest  expan- 
sion, the  examiner  should  stand  at  the  subject's  side,  placing  one 
hand  upon  the  sternum  and  the  other  between  the  scapulae. 


Fig-  75- — Technic  of  palpating  the  pulmonary  apices. 

Vocal  Fremitus. — Vocal  fremitus  is  the  tactile  vibration  appre- 
ciated by  the  hand  applied  to  the  chest-wall  while  the  patient  is 
speaking  aloud.  The  vibrations  thus  felt  arise  in  the  vocal  cords, 
whence  they  travel  via  the  trachea,  the  bronchi,  the  vesicular  structure, 
and  the  parietes  to  the  surface  of  the  thorax,  where  they  are  recog- 
nized as  a  peculiar  purring  vibratory  sensation. 

In  eliciting  vocal  fremitus  the  palm  of  the  hand  is  pressed  firmly 
against  the  bared  chest  of  the  patient,  who  is  instructed  to  repeat, 
in  a  deep  voice,  "ninety-nine,"  or  to  count  "one,  two,  three"  a  number 
of  times,  the  resulting  vibrations  being  appreciated  by  the  palmar 
surfaces  of  the  examiner's  fingers.  Or,  as  Berkeley  suggests,  the 
sound  of  "66,"  as  in  "moon"  or  "rood,"  is  excellent  for  tactile 
purposes.  Ulnar  palpation,  or  the  application  of  the  ulnar  side  of 


132  PHYSICAL   DIAGNOSIS 

the  hand,  is  recommended  by  some  clinicians,  but  it  seems  far  infe- 
rior to  the  palmar  method,  owing  to  the  much  less  delicate  tactile  sen- 
sibility of  the  side  of  the 
hand  as  compared  to  that 
of  the  fingers.  Comparative 
tests  of  the  fremitus  of  both 
halves  of  the  chest  should 
always  be  practised,  in  order 
to  detect  slight  differences. 
The  intensity  of  the  vibra- 
tions depends  upon  the  loud- 
ness  and  the  pitch  of  the 
voice,  and  upon  the  conduct- 
ing qualities  of  the  structures 
between  the  larynx  and  the 
palpator's  hand.  It  is  more 
intense  in  adults  than  in 
children;  in  men  than  in 
women;  in  persons  of  loud, 
low-pitched,  harsh  voice  than 

Lin  those  whose  voice  is  quiet, 
high-pitched,  and  soft;  and 
'jHl      in  the  thin,  spare  individual 

Fig.  76. — Comparative  intensity  of  vocal  than  in  one  whose  chest  is 
fremitus,  vocal  resonance,  and  respiratory  <  e  .  , 

sounds  over  the  anterior  thorax.  muscular,  fat,  or  edematous. 

The    comparative    intensity 

of  vocal  fremitus  over  different  regions  of  the  chest  is  shown  by 
Figs.  76  and  77. 

Normally,  vocal  fremitus  is  relatively  exaggerated  over  the  right 
side  of  the  thorax,  especially  in  the  infraclavicular  and  interscapular 
regions.  This  disparity  between  the  fremitus  of  the  two  sides  is 
explained  partly  by  the  larger  caliber  and  the  less  acute  bronchotrach- 
eal  angle  of  the  right  bronchus,  and  partly  by  the  fact  that  the  tube 
leading  to  the  right  upper  lobe  arises  closer  to  the  trachea  and  at  a 
higher  point  than  the  corresponding  left  tube — anatomic  differences 
by  virtue  of  which  the  volume  of  vibrations  is  greater,  their  route 
shorter,  and  their  transmission  less  impeded  within  the  bronchus  of 
the  right  lung  than  within  that  of  the  left.  The  intimate  anatomic 
relation  of  the  trachea  and  the  right  lung  is  another  factor  of  right- 
sided  exaggeration  of  the  fremitus,  as  recently  shown  by  Fetterolf. 
Lateral  decubitus  also  influences  the  intensity  of  the  voice  vibra- 
tions, the  side  of  the  chest  in  contact  with  the  bed  affording  a 
perceptible  increase  of  both  vocal  fremitus  and.  resonance,  together 


EXAMINATION   OF    THE    BRONCHOPULMONARY   SYSTEM 


with  a  commensurate  modification  of  pulmonary  percussion  reso- 
nance and  a  slight  exaggeration  of  the  respiratory  murmur. 

The  vocal  fremitus  is  faint  over  the  scapulae,  the  sternum,  and 
the  female  mammae,  owing  to  the  interference  of  these  parts  with  the 
conduction  of  the  vibratory  waves.  These  latter  are,  of  course, 
absent  over  the  areas  of  the  thorax  corresponding  to  the  immediate 
contact  of  the  heart,  liver,  and  the  spleen.  On  the  other  hand, 
the  voice  vibrations  are  clearly  conducted  by  the  clavicle,  and  can 
be  distinctly  palpated  as  far  as  its  outer  extremity. 

Increased  Vocal  Fremitus. — This  is  found  in  croupous  pneumonia, 
diffuse  catarrhal  pneumonia,  tuberculous  infiltration,  infarction, 
and  fibrosis,  since  consolida- 
tions such  as  these  conduct 
vibrations  with  undue  power; 
the  same  thing  occurs  in  the 
case  of  a  dense  intrathor- 
acic  neoplasm  situated  near  a 
bronchus.  An  interpleural 
fibrous  band  will  telephone 
voice  fremitus  through  a 
pleural  effusion,  notwithstand- 
ing the  non-conducting  prop- 
erties of  the  latter  (v.  i.) .  In- 
creased pulmonary  tension, 
which  favors  clear  transmis- 
sion of  the  sound-waves,  ex- 
plains the  exaggerated  frem- 
itus incident  to  congestion  of 
the  lungs.  A  cavity,  either 


: 


pulmonary  or  bronchial,  am- 
plifies the  voice  vibrations 
and,  therefore,  increases  the 
fremitus,  but  to  act  thus  as 
a  resonating  chamber  the 
cavity  must  be  near  the  surface 
and  of  considerable  size,  with 
resilient  walls  and  a  patent 
bronchial  communication. 

Decreased  Vocal  Fremitus. — Modifications  of  vocal  fremitus, 
ranging  from  slight  enfeeblement  to  actual  abolition  of  the  vibrations, 
occur  as  the  result  of  subnormal  pulmonary  tension,  pleural  effusions 
and  thickening,  and  bronchial  obstruction.  Hypertrophic  emphy- 
sema, which  diminishes  the  tension  and  the  resiliency  of  the  lungs, 


Fig.  77. — Comparative  intensity  of  vocal 
fremitus,  vocal  resonance,  and  respiratory 
sounds  over  the  posterior  thorax. 


134  PHYSICAL   DIAGNOSIS 

weakens  the  transmission  of  the  voice  vibrations,  but  scarcely  to  the 
extent  popularly  supposed,  and,  by  a  similar  mechanism,  pulmonary 
edema  has  the  same  effect  on  fremitus.  A  plural  cavity  containing 
either  air  or  liquid  interferes  with  vocal  fremitus,  in  consequence  of 
the  non-conducting  properties  of  the  effusion  and  because  of  the 
associated  pulmonary  relaxation.  A  greatly  thickened  pleura  or 
one  bathed  in  a  thick,  buttery  exudate  also  weakens  the  vocal  vibra- 
tions. If  any  part  of  the  bronchial  tubes  be  blocked,  the  vocal  fre- 
mitus over  the  pulmonary  area  communicating  with  the  occluded  part 
of  the  bronchial  tree  is  correspondingly  diminished.  This  occurs 
as  the  result  of  spasm  of  the  tubes,  inflammatory  swelling  of  their 
mucosa,  and  mechanical  obstruction  of  their  lumen  by  a  foreign 
body  or  by  the  pressure  of  an  aneurism,  a  neoplasm,  or  a  glandular 
mass.  Or  the  occlusion  may  be  spastic  or  exudative,  as  in  diffuse 
catarrhal  bronchitis,  fibrinous  bronchitis,  and  asthma.  It  is  import- 
ant to  note  that  in  croupous  pneumonia,  despite  the  consolidation, 
vocal  fremitus  may  be  completely  abolished  over  the  pneumonic 
lobe  if  the  bronchus  leading  thereto  happens  to  be  plugged  with  a 
mass  of  fibrin. 

Rhonchal  Fremitus. — The  vibrations  of  coarse  bronchial  and 
tracheal  rales  are  sometimes  felt  upon  the  surface  of  the  chest,  especi- 
ally during  inspiration.  This  rhonchal  or  bronchial  fremitus  is  to  be 
looked  for  in  bronchitis  and  in  asthma,  and  is  particularly  common 
in  the  bronchitis  of  young  children.  It  is,  of  course,  abolished  by 
bronchial  occlusion,  and  is  influenced  by  coughing  and  by  deep 
respiration.  Occasionally  tactile  fremitus  due  to  cavernous  rales 
is  appreciable  over  pulmonary  and  bronchial  cavities. 

Succussion  Fremitus. — This  sign,  the  tactile  equivalent  of  the 
Hippocratic  succussion  sound,  may  occur  over  a  pleural  cavity  con- 
taining air  and  fluid  when  the  subject's  chest  receives  a  sudden  jar, 
so  as  to  splash  a  wave  of  fluid  against  the  inner  chest-wall. 

Tussile  Fremitus. — The  palpable  vibrations  excited  by  coughing 
are  known  as  tussile  or  tussive  fremitus.  They  are  of  trifling  clinical 
value,  save  perhaps  in  cases  of  aphonia,  in  which  it  is  impossible  to 
elicit  vocal  fremitus. 

Friction  Fremitus. — Tactile  vibrations  corresponding  to  the 
pleural  friction-sound  are  sometimes  detected  over  roughened  pleural 
surfaces  when  the  patient  takes  a  deep  breath.  This  pleural  friction 
fremitus  feels  superficial  to  the  palpating  hand,  is  affected  by  firm 
pressure  and  by  forcible  respiration,  and  has  a  fine,  rasping,  or  even 
creaking  quality,  according  to  the  character  of  underlying  pleural 
\esion.  (Cf.  Pericardial  Friction,  p.  389.) 

Increased  Resistance  and  Fluctuation. — The  increased  surface 


EXAMINATION    OF    THE    BRONCHOPULMONARY   SYSTEM     135 

resistance  over  pleural  thickening,  pleural  effusions,  and  pulmonary 
consolidations  is  appreciable  by  palpation  as  well  as  by  percussion. 
Less  commonly  the  resistance  is  increased  by  the  diminished  elasticity 
of  the  lungs  incident  to  extreme  emphysema  and  to  pneumothorax. 
Increased  rigidity  of  the  thoracic  parietes  causes  a  corresponding 
increase  in  the  degree  of  resistance  upon  the  surface. 

In  exceptional  cases  pitting  and  even  circumscribed  fluctuation 
due  to  an  affection  of  the  lungs  or  pleura  can  be  felt  upon  the  surface 
of  the  thorax,  as  in  the  preperforative  stage  of  empyema  necessitatis, 
and  in  pulmonary  hydalid  cyst,  inflamed  and  about  to  fistulate  through 
the  chest-wall.  Under  the  latter  circumstance  hydatid  fremitus 
is  sometimes  demonstrable  by  laying  the  fingers,  widely  separated, 
over  the  swelling,  and  sharply  percussing  upon  one  of  them,  where- 
upon a  delicate  thrill,  due  to  the  impact  of  the  daughter  cysts,  is 
appreciated  by  the  other  three  fingers.  This  so-called  hydatid 
fremitus  or  thrill  must  be  distinguished  from  muscular  fremitus 
(Barnabei)  arising  from  fibrillary  muscular  contractions  set  up  by 
manual  stimulation.  Such  fremitus  is  especially  prone  to  occur  in 
the  abdominal  muscles  in  connection  with  conditions  of  excessive 
intraperitoneal  tension,  and,  unlike  true  hydatid  fremitus,  can  be 
excited  at  will,  merely  by  deep,  kneading  palpation. 

PERCUSSION 

Percussion  of  the  lungs  gives  information  relating  to  the  extent 
of  the  pulmonary  or  vesicular  resonance  and  its  pathologic  modifica- 
tions, due  to  lesions  of  the  lungs  and  their  pleural  investment,  such 
lesions  including  consolidation,  collapse,  overdistention,  and  excava- 
tion of  the  vesicular  structure,  together  with  pleural  thickening  and 
collections,  gaseous  or  fluid,  within  the  pleural  sacs. 

The  general  rules  regarding  the  patient's  symmetric  posture, 
muscular  relaxation,  and  quiet  respiration  (see  p.  27)  are  to 
be  observed,  in  order  successfully  to  practise  pulmonary  percus- 
sion. In  examining  a  bed-ridden  person  perfect  anatomic  sym- 
metry of  the  parts  is  a  preliminary  essential  to  the  best  results,  whether 
the  subject  be  in  the  dorsal,  the  ventral,  or  the  lateral  decubitus. 
In  percussing  the  anterior  chest-wall  of  a  patient  in  the  upright 
position  his  head  should  be  kept  in  the  median  line,  with  the  arms 
hanging  naturally  at  the  side,  so  as  to  poise  the  trunk  symmetrically 
(Fig.  i) .  In  percussing  the  back  the  subject  should  bend  well  forward 
from  the  waist,  and  fold  the  arms  across  the  chest,  in  order  to  tilt 
forward  the  scapulae,  thus  flattening  the  posterior  thoracic  wall  and 
exposing  as  large  an  area  of  it  as  possible;  or  the  patient  may  lean 


136  PHYSICAL   DIAGNOSIS 

forward  in  the  position  illustrated  below  (Fig.  78).  The  lateral 
regions  of  the  thorax  are  made  accessible  by  having  the  subject  raise 
the  arms,  with  the  clasped  hands  resting  upon  the  top  of  the  head. 
Percussion  of  the  apices  is  not  an  easy  matter,  owing  chiefly  to  the 
dulling  effect  of  the  thick  musculature  of  the  neck,  and  to  the  adja- 
cent tympanicity  of  the  trachea.  The  apices  may  be  percussed  from 
before,  with  the  little  finger  applied  as  a  pleximeter  to  the  supra- 
clavicular  space  above  and  parallel  to  the  clavicle  (Fig.  79),  or  from 
behind,  with  the  pleximeter  finger  pointing  toward  the  sternoclavic- 
ular  joint  (Fig.  80). 

In  comparative  percussion  the  areas  to  be  contrasted  should  be 
percussed  during  the  same  respiratory  stage,  the  force  of  the  blow, 


Fig.  78. — Technic  of  percussing  the  posterior  thorax. 


the  pressure  of  the  pleximeter  finger,  and  the  other  details  of  the 
percussion  technic  being  identical.  Furthermore,  the  comparable 
parts  must  be  of  similar  anatomic  structure — the  sound  obtained 
over  an  interspace  should  be  compared  with  that  elicited  over  a 
corresponding  interspace,  not  with  the  sound  over  a  rib  or  over  a 
dense  muscle. 

By  respiratory  percussion  certain  respiratory  differences  in  the  per- 
cussion sounds  can  be  judged  by  percussing  over  the  same  area  while 
the  subject  holds  the  breath,  first,  after  deeply  inflating,  and  then 
after  similarly  deflating,  the  lungs.  Normally,  when  the  breath  is 
held  after  a  full  inspiration,  the  sound  is  of  greater  resonance,  more 
volume,  and  higher  pitch  than  that  elicited  after  a  forced  expiration, 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM       137 

these  differences  being  particularly  clear  on  the  right  side,  below  the 
clavicle  and  above  the  scapula. 

Normal  Pulmonary  or  Vesicular  Resonance. — The  distinctive 
hall-mark  of  pulmonary  resonance  is  its  quality,  which,  being  sui 
generis,  is  comparable  only  to  the  sound  excited  by  the  vibration  of 
healthy  pulmonary  tissue  having  an  air-content  distributed  through 
innumerable  minutely  divided  alveolar  spaces.  Experience  alone 


Fig.   79-— Technic  of  percussing  the  pulmonary  apices. 

will  enable  one  to  recognize  this  characteristic  vesicular  quality,  which 
dominates  the  pulmonary  percussion  sound,  irrespective  of  its  pitch, 
intensity,  and  duration.  These  acoustic  details  of  resonance  have 
been  considered  in  a  preceding  section.  (See  p.  17.) 

Certain  regional  differences  in  normal  pulmonary  resonance,  due 
entirely  to  physiologic  causes,  must  be  clearly  distinguished,  in  order 
not  to  misinterpret  the  results  of  percussion  of  the  lungs.  Modifica- 
tions of  the  percussion  sound,  perfectly  normal  in  one  region  of  the 


138 


PHYSICAL    DIAGNOSIS 


chest,  may  be  pathologic  when  found  in  a  different  area,  so  that  the 
significance  of  any  given  sound  rests  upon  its  variance  from  the  sound 
afforded  by  the  part  in  health. 

The  clear,  low  pitch  and  vesicular  quality  of  pulmonary  resonance 
are  typically  illustrated  by  percussing  in  the  upper  axillary  region 
above  the  fourth  rib,  and  this  is  also  true  of  the  middle  of  the  infra- 
clavicular  region;  at  the 
sternal  end  of  this  region, 
however,  the  resonance 
of  the  lung  blends  with 
the  osteal  tone  of  the 
sternum  and  with  the 
tympanitic  element  of 
the  underlying  primary 
bronchi  and  trachea. 
Owing  to  the  anatomic 
peculiarities  of  the  right 
bronchus  and  to  the 
encroachment  of  the 
large  blood-vessels  upon 
the  right  pulmonary 
apex  (Norris;  Fetterolf), 
the  percussion  sound 
is  somewhat  higher 
pitched  and  less  typically 
vesicular  in  the  right 
than  in  the  left  infra- 
clavicular  area.  To  a 
minor  degree  these  differ- 
ences are  also  found  in  the  supraclavicular  regions,  at  the  inner 
portions  of  which  one  must  reckon  with  tracheal  tympany. 

Anteriorly,  on  the  right  side,  the  dulling  effect  of  the  liver  is  encoun- 
tered in  the  midclavicular  line  below  the  fourth  rib,  and  in  the  anterior 
axillary  line  below  the  sixth  rib.  On  the  left  side,  below  the  fourth 
rib,  the  dulness  of  the  heart  modifies  the  pulmonary  sound  within  the 
midclavicular  line,  while  between  thjs  line  and  the  axilla  the  influence 
of  gastric  tympany  is  apparent  below  the  fifth  rib.  On  both  sides 
resonance  is  obscured  over  the  site  of  the  great  pectoral  muscles 
and  the  mammary  glands.  Laterally,  hepatic  dulness  on  the  right 
side,  and  gastric  tympany  (perhaps,  also,  splenic  dulness)  on  the  left 
side,  modify  the  resonance  of  the  lower  axillae.  Posteriorly,  the 
percussion  sound  is  nowhere  so  resonant  as  it  is  anteriorly,  this  being 
especially  noticeable  above  and  over  the  scapulae,  where  the  dead- 


Fig.  80. — Technic  of   percussing  the    pulmonary 
apices. 


EXAMINATION    OF    THE    BRONCHOPULMONARY    SYSTEM      139 

ening  effect  of  the  bone  is  obvious.  In  the  other  regions  of  the  back 
resonance  is  more  or  less  obscured  by  the  thick  musculature,  the 
spine,  and  the  underlying  solid  viscera. 

Aside  from  the  foregoing  differences,  it  must  be  remembered  that 
pulmonary  resonance  is  obscured  wherever  the  thorax  bears  a  dense 
investment  of  muscle  or  of  fat,  and  also  that  undue  rigidity  of  the 
bony  thorax  lends  impurity  to  the  percussion  sound.  Postural 
compression  of  one  side  of  the  thorax  may  cause  dulness  due  to 
mechanical  suppression  of  parietal  vibrations.  (See  p.  133.) 

Normal  Limits  of  the  Pulmonary  Borders  (Figs.  71,  72,  73, 
and  74) . — The  position  of  the  pulmonary  borders  is  determined  by 
percussion  while  the  subject's  lungs  are  in  a  state  of  median  inflation, 
i.  e.,  during  respiratory  repose.  The  upper  borders  are  outlined  by 
percussion  over  the  supraclavicular  spaces,  where  the  apices  project, 
in  health,  from  £  to  i£ inches  (1.25  to  3.75  cm.)  above  the  clavicles. 
The  lower  borders  are  mapped  out  by  percussing  vertically  downward 
along  the  midclavicular,  the  midaxillary,  and  the  scapular  lines,  from 
typical  pulmonary  resonance  to  the  levels  of  hepatic  flatness  on  the 
right  side,  and  to  gastric  tympany  and  the  flatness  of  the  spleen,  the 
kidney,  and  the  lumbar  muscles  on  the  left  side.  The  lower  border 
of  the  right  lung  extends  to  the  sixth  rib  in  the  midclavicular  line,  to 
the  eighth  rib  in  the  midaxillary  line,  and  to  the  tenth  rib  in  the  scapu- 
lar line,  hepatic  flatness  lying  below  these  levels.  The  lower  border 
of  the  left  lung  extends  in  the  midclavicular  line  to  the  sixth  rib  or 
interspace,  below  which  there  is  the  sound  of  gastric  tympany,  while 
the  lateral  and  the  posterior  levels  of  the  left  lower  border  are  prac- 
tically the  same  as  those  of  the  right  lung.  The  anterior  borders  of 
the  lungs  are  too  closely  approximated  to  be  separated  by  percussion, 
and  the  excessive  vibrations  of  the  sternum,  beneath  which  these 
borders  lie,  also  forbid  their  delimitation.  The  peculiar  curve  of 
the  precordial  border  of  the  left  lung  bounds  the  area  of  cardiac 
flatness  lying  at  the  left  sternal  margin,  between  the  fourth  and  sixth 
ribs.  (See  Cardiac  Percussion,  p.  350.) 

In  early  childhood  the  lower  pulmonary  borders  are  higher,  and 
in  advanced  life  lower,  than  the  above  mean  levels,  the  difference  in 
each  instance  amounting  to  about  i  inch  (2.5  cm.).  Changing  from 
the  dorsal  to  the  lateral  decubitus  depresses  the  lower  border  of  the 
uppermost  lung  about  i^  inches  (3.75  cm.)  in  the  axilla,  and  changing 
from  the  dorsal  to  the  erect  posture  elevates  the  lower  level  J  inch 
(1.25  cm.)  anteriorly. 

Changes  in  the  Mobility  and  Position  of  the  Pulmonary 
Borders. — The  mobility  of  the  lungs  is  gaged  by  the  excursions  of 
the  pulmonary  borders,  as  shown  by  their  positions  during  extreme 


140  PHYSICAL    DIAGNOSIS 

inspiration  and  expiration.  In  the  healthy  adult  the  vertical  excursion 
of  the  lower  border  above  and  below  the  mean  is  about  i£  inches 
(3.75  cm.)  anteriorly,  and  3  inches  (7.5  cm.)  laterally,  the  inspiratory 
convergence  of  the  anterior  borders  encroaching  upon  precordial 
flatness  practically  to  the  point  of  obliteration.  Restriction,  in  part 
or  absolute,  of  this  excursion  is  noted  should  the  lungs  be  overdis- 
tended,  infiltrated,  or  hampered  by  adhesions  or  by  mechanical 
pressure.  Thus,  emphysema,  consolidations,  fibrosis,  adhesive 
pleurisy,  and  excessive  intra-abdominal  pressure,  by  limiting  the 
normal  pulmonary  excursions,  are  attended  by  unnaturally  small 
differences  between  the  inspiratory  and  the  expiratory  levels  of  the 
pulmonary  borders,  and  in  such  instances  the  axillary  diaphragm 
shadow  is  correspondingly  obliterated.  (See  Litten's  Sign,  p.  93.) 

The  extent  of  the  pulmonary  resonance  is  determined  by  the 
position  of  the  pulmonary  borders  during  respiratory  repose,  devi- 
ations from  the  normal  boundaries  being  either  general  or  circum- 
scribed, according  to  the  nature  of  the  pulmonary  lesion  responsible 
for  such  changes. 

A  general  extension  in  the  area  of  pulmonary  resonance  is  met  with 
in  hypertrophic  emphysema,  in  which  all  the  normal  boundaries 
of  the  lungs  are  overstepped,  the  apical  resonance  rising  to 
an  unnatural  height  above  the  clavicles,  the  basic  resonance  encroach- 
ing upon  the  upper  zone  of  hepatic  dulness,  and  the  resonance  of 
the  anterior  borders  extending  partly  or  completely  over  the  cardiac 
area  ordinarily  uncovered  by  the  lungs.  It  is  in  this  region  especially 
that  an  emphysematous  extension  of  the  borders  is  likely  to  be  most 
readily  detected.  A  similar  extension  of  the  pulmonary  borders 
may  attend  an  asthmatic  paroxysm,  fibrinous  bronchitis,  and  dilata- 
tion of  the  lungs  consequent  to  uncompensated  cardiac  disease. 
Circumscribed  emphysema  is  associated  with  extension  of  the  pul- 
monary resonance  corresponding  in  situation  and  extent  to  the  seat 
of  the  lesion.  The  lower  pulmonary  borders  not  uncommonly  sag 
below  their  normal  level  in  Gle"nard's  disease. 

Decrease  in  the  extent  of  pulmonary  resonance,  if  general,  may  be 
symptomatic  of  atrophic  emphysema;  if  local,  some  lesion  provoca- 
tive of  pulmonary  retraction  and  shrinkage  is  suggested.  Diminu- 
tion in  the  height  of  the  apical  resonance,  unilateral  or  bilateral, 
points  to  phthisis  or  to  pleural  adhesion.  Elevation  of  the  lower 
borders,  with  apparent  extension  of  the  vertical  hepatic  dulness,  may 
be  symptomatic  of  pleural  retraction  or  of  tuberculous  or  atelectatic 
contraction  of  the  lung.  Unilateral  elevation  of  the  lower  pulmonary 
border  is  also  observed  in  pneumothorax,  pleurisy  with  effusion, 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM      141 


paralysis  of  the  diaphragm,  and  upward  displacement  of  this  muscle 
by  excessive  subphrenic  pressure.  Fibroid  retraction  affecting  the 
anterior  borders  of  the  lungs  may  account  for  an  unduly  large  area 
of  cardiac  dulness. 

Dulness  and  Flatness. — Impaired  pulmonary  resonance,  with 
a  corresponding  increase  in  resistance,  denotes  airlessness,  absolute 
or  relative,  in  the  structures  within  range  of  the  percussion  impact, 
or,  as  Weil  expresses  it,  the  acoustic  sphere  of  action.  This  may  be 
due  to  infiltration  of  the  pulmonary  parenchyma,  to  fluid  within  the 
pleural  sac,  to  thickening  of  the  pleura,  or  to  a  neoplasm  situated 
directly  beneath  the  chest-wall.  Thus,  dulness  is  found  in  croupous 
pneumonia,  diffuse  coalescing  catarrhal  pneumonia,  phthisis,  atelecta- 


Bronchovesicular6rtal/iiry 
Increased  oocal  fremt(us_ 
Jnereaseal  uocal  resonance 
Impaired  high-bitched 
1  resomuuae 

Bronchial  brealhwy  _ 
Increased  oocalfremitus. 
increased  vocal  resonance 
JJu.1  ness. 

Jlbsent  breathing 
Absent  uocai  fremitiu 
Absent  vocal  resonanee. 


,  ronchial  Ireatking. 
Increased  vocal fremitus. 


Fig.  81. — Physical  signs  in  pulmonary  consolidation  and  in  pleural  effusion. 

sis,  congestion,  edema,  cirrhosis,  and  in  destructive  processes  of  the 
lung,  such  as  abscess,  gangrene,  and  new-growths.  The  percussion 
sound  is  dulled  to  the  degree  of  flatness  as  the  result  of  pleural  effusion, 
pleural  thickening,  enlarged  bronchial  glands,  and  neoplasms  of  the 
pleura  and  of  the  mediastinum  (Fig.  81). 

The  degree  of  dulness  depends  upon  the  volume  of  air  in  the  parts 
percussed,  upon  their  size  and  situation,  and  upon  the  force  of  the 
percussion  stroke.  Other  things  being  equal,  the  larger,  more  super- 
ficial, and  more  densely  consolidated  the  lesion,  the  more  marked  the 
degree  of  dulness.  The  influence  of  the  above  factors  is  well  shown 
by  comparing  the  sounds  produced  by  strong  and  by  light  percussion 
over  pulmonary  infiltrations  of  different  size,  situation,  and  distribu- 


142 


PHYSICAL   DIAGNOSIS 


tion  (Fig.  82).  The  percussion  stroke  may  be  too  light  to  elicit 
the  dulness  of  a  deeply  seated  extensive  consolidation,  since  with 
light  percussion  the  vibrations  fail  to  reach  the  airless  area  and, 
therefore,  elicit  only  the  resonance  of  the  intervening  normal  vesicular 
structure.  Strong  percussion,  the  sphere  of  which  includes  the  con- 
solidated patch,  at  once  reveals  the  latter  by  an  impairment  of  the 


Consolidation. 


LIVER 


^Consolidation  Sfay  &**&» 

'?     LUNG  Rvlonanct} 


Fig.  8a. — The  effects  of  variable  percussion  force. 

resonance.  Percussion  may  be  too  strong  to  bring  out  the  dulness 
of  a  small  superficial  infiltration,  should  the  blow  be  of  sufficient  force 
to  set  up  vibrations  in  the  lung  tissue  behind  and  around  the  patch, 
the  dulness  of  which  is  thus  obscured  by  the  predominant  resonance 
of  the  vesicular  sound.  Under  the  same  circumstance,  if  the  per- 
cussion stroke  be  light,  so  as  to  affect  only  the  infiltrated  area,  the 
latter's  dulness  will  be  demonstrable.  Neither  light  nor  strong  per- 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM       143 

cussion  may  avail  in  eliciting  the  dulness  of  diffuse  disseminated 
areas  of  infiltration,  owing  to  the  prevailing  resonance  of  the  sur- 
rounding pulmonary  tissue,  whereby  the  dulness  is  so  effectually 
masked  that  it  escapes  notice.  This  is  particularly  true  if  strong 
percussion  be  made,  for  the  more  forcible  the  blow,  the  more  intense 
the  vesicular  vibrations.  Analogous  to  this  is  the  neutralization  of 
dulness  from  consolidation  by  the  undue  resonance  of  the  adjacent 
relaxed  or  vicariously  distended  lung. 

The  situation  of  a  dull  or  a  flat  area  has  a  certain  clinical  bearing 
upon  the  character  of  the  underlying  lesion,  although  deductions 
based  upon  such  a  premise  are  to  be  made  only  in  correlation  with 
other  physical  signs.  Thus,  apical  impairment  of  the  percussion  sound 
is  most  suggestive  of  tuberculosis;  equality  of  the  sound  at  both  apices 
points  to  an  incipient  left-sided  infiltration,  since  in  health  the  upper 
right  lobe  shows  relative  impairment.  (Seep.  126.)  A  second  important 
factor  of  apical  dulness  is  the  so-called  apex  pneumonia,  which  occurs 
especially  in  children.  Sternal  and  parasternal  dulness,  generally 
near  Louis'  angle,  is  found  in  mediastinal  tumors  large  enough  to 
have  encroached  anteriorly  upon  the  inner  surface  of  the  sternum, 
and  laterally  upon  the  anterior  borders  of  the  lungs.  The  dulness 
of  tumors  of  the  lungs  and  the  pleura  cannot  be  referred  definitely 
to  any  distinct  topographic  region.  Dulness  or  flatness  at  the  base 
posteriorly,  if  not  obviously  due  to  enlargement  of  the  liver  or  the 
spleen,  is  commonly  a  sign  of  croupous  pneumonia,  fluid  within  the 
pleural  cavity,  and  pulmonary  edema,  infarction,  or  hypostatic  con- 
gestion. Basal  flatness  shifting  with  the  subject's  change  of  posture 
occurs  in  pleural  transudates,  such  as  hydrothorax  and  hemothorax; 
rarely,  if  ever,  does  an  inflammatory  pleural  exudate  gravitate  in 
this  manner.  Para-vertebral  dulness,  if  bilateral,  should  prompt  a 
search  for  atelectasis  and  its  exciting  factors,  or  for  hydrothorax.  In 
pleural  effusion  a  triangular  patch  of  paravertebral  dulness  above 
the  level  of  the  twelfth  rib  may  be  demonstrable  on  the  unaffected 
side — Grocco's  sign.  (See  p.  273.)  Impairment  in  the  interscap- 
ular  area  is  significant  of  enlargement  of  the  bronchial  glands,  as 
well  as  of  aneurism  of  the  descending  aorta,  which  causes  dulness 
between  the  vertebral  column  and  the  left  scapula.  Dulling  of  the 
normal  tympany  in  Traube's  space  may  be  due  to  fluid  within  the 
left  pleural  sac,  and  to  enlargements  of  the  heart,  liver,  or  spleen, 
while  in  pericardial  effusion,  adhesive  pericarditis,  right  pleural  effu- 
sion, pleural  thickening,  and  basal  pneumonia  the  normal  resonance 
of  Ebstein's  cardiohepatic  angle  may  be  obliterated.  Dulness  in  the 
axilla  is  commonly  a  sign  of  pulmonary  infarction. 


144 


PHYSICAL    DIAGNOSIS 


Unilateral  dulness,  of  a  peculiar  wooden  quality,  over  the  greater 
part  of  one  lung,  is  often  met  with  in  pulmonary  cirrhosis,  and  mul- 
tiple patches  of  impaired  resonance  are  sometimes  to  be  detected  in 
catarrhal  pneumonia,  miliary  tuberculosis,  and  pulmonary  syphilis. 

Hyperresonance  and  Tympany. — Exaggeration  of  pulmonary 
resonance  indicates  that  the  structures  within  the  percussion  sphere 
contain  an  abnormally  large  volume  of  air,  that  their  mural  tension 
is  altered,  or  that  they  conduct  clearly  the  hyperresonance  of  adjacent 
air-containing  parts,  according  to  the  character  of  the  exciting  cause 
of  the  altered  sound.  Thus,  hyperresonance  is  met  with  as  the  result 
of  vesicular  emphysema,  bronchopulmonary  cavities,  pneumothorax, 


rresonaMx. 


Tympany 


Fig-  83. — The  effect  of  pulmonary  cavities,  pneumothorax,  and  emphysema  upon 
the  percussion  sound. 

parabronchial  consolidations,  and  pulmonary  relaxation  consequent 
to  mechanical  or  to  parenchyma tous  changes  (Fig.  83). 

The  increased  resonance  of  hypertrophic  emphysema,  dubbed 
"band-box  resonance,"  is  explained  by  the  unduly  excessive  volume 
of  air  within  the  lungs,  and  by  the  state  of  pulmonary  relaxation  due 
to  permanent  overdistention  and  destruction  of  the  alveolar  tissue. 
In  the  condition  termed  compensatory  emphysema  hyperresonance 
is  elicited  over  the  lung  vicariously  dilated  in  consequence  of  crippling 
of  the  opposite  lung.  The  exaggerated  resonance  expressive  of  these 
emphysematous  changes  is  a  commingling  of  the  vesicular  and  the 
tympanitic  qualities,  of  abnormally  increased  intensity  and  duration, 
and  of  a  pitch  rising  in  proportion  to  the  predominance  of  the  tym- 
panitic quality — the  vesiculotympanitic  resonance  of  Flint.  Acoustic- 


EXAMINATION    OF    THE    BRONCHOPULMONARY    SYSTEM       145 

ally,  this  sound  is  essentially  similar  to  the  resonance  of  Skoda, 
described  below. 

Pulmonary  hyperresonance  commonly  accompanies  the  extremes 
of  life — as  in  the  young  child,  whose  lungs,  owing  to  their  great 
elasticity,  are  prone  to  temporary  dilatation  from  simple  respira- 
tory overaction,  as,  for  example,  during  a  fit  of  crying;  and  in  the 
very  aged,  whose  lungs,  in  consequence  of  senile  changes,  are  in  a 
state  of  relaxation.  In  scoliosis  circumscribed  patches  of  compensa- 
tory hyperresonance  may  be  found  opposite  to  the  vertebral  con- 
vexity (Gray). 

Conditions  of  pulmonary  relaxation  secondary  to  compression  and 
to  parenchymatous  disease  of  the  lungs  may  account  for  a  decided 
increase  in  the  resonance  of  the  percussion  sound,  owing  to  the 
diminished  tension  of  the  vesicular  tissues.  This  sort  of  hyper- 
resonance, termed  Skodaic  resonance,  is  elicited  by  percussion  over 
the  compressed  lung  immediately  above  a  pleural  effusion  or  an 
extensive  basal  pneumonia;  less  readily  it  can  be  detected  over  the 
relaxed  pulmonary  tissue  adjacent  to  an  intrathoracic  neoplasm,  an 
enlarged  heart,  or  a  large  pericardial  effusion.  Upward  displace- 
ment of  the  diaphragm,  secondary  to  excessive  intra-abdominal 
pressure,  crowds  the  lungs  upward  and  lowers  their  tension  to  a 
degree  provocative  of  greatly  exaggerated  resonance.  In  the  for- 
mative stage  of  obstruction  atelectasis  hyperresonance  is  found  over 
the  area  corresponding  to  the  patch  of  airless  relaxed  lung.  In 
acute  febrile  states  a  general  hyperresonance,  presumably  due  to 
diminished  pulmonary  tension  of  toxic  origin,  has  been  described 
by  Samuel  West  as  an  "acute  pulmonary  tympanites." 

Hyperresonance  dependent  upon  parenchymatous  changes  in  the 
lungs  develops  in  the  congestive  stage  of  croupous  pneumonia,  in 
pulmonary  edema,  and  in  pulmonary  infarction,  all  of  which  lesions 
lower  the  tension  of  the  vesicular  structure. 

It  should  be  borne  in  mind  that  the  hyperresonance  observed  in 
the  foregoing  conditions  is  incidental  only  to  the  stage  of  pulmonary 
relaxation,  for  when  the  affected  lung  becomes  consolidated,  dulness 
at  once  appears.  This  transition  from  hyperresonance  to  dulness 
occurs,  for  example,  in  compression  atelectasis  so  soon  as  the  vesicular 
structure  becomes  infiltrated  or  carnified,  and  in  croupous  pneumonia 
when  the  stage  of  red  hepatization  sets  in. 

Pulmonary  and  bronchiectatic  cavities,  inasmuch  as  they  act  as 
air-containing  resonating  chambers,  furnish  a  tympanitic  percussion 
sound  whose  tonal  characteristics  vary  with  the  physical  properties 
of  the  excavation  and  the  adjacent  parts.  It  is  important  to  under- 
stand that  a  cavity  affords  typical  physical  signs  only  when  it  is  super- 


146  PHYSICAL   DIAGNOSIS 

ficial,  filled  with  air,  and  resilient,  with  a  free  bronchial  outlet.  A 
large  cavity  may  be  so  deeply  buried  in  the  parenchyma  of  the  lung 
as  to  escape  recognition,  even  by  the  most  vigorous  percussion;  while 
a  much  smaller  cavity,  if  it  be  superficial,  can  generally  be  detected 
by  gentle  percussion.  When  the  air  within  a  cavity  is  replaced  by 
liquid,  the  primary  tympany  changes  to  flatness,  which  becomes  more 
and  more  marked  as  the  resonating  chamber  of  the  cavity  is  thus 
abolished.  Should  the  cavity  be  emptied  by.  expectoration,  the 
primary  tympany  reappears,  and  a  similar  transition  from  tympany 
to  flatness  to  tympany  may  occur  as  the  result  of  the  lodgment  and 
the  dislodgment  of  a  tight  mucous  plug  in  the  cavity's  bronchial 
outlet.  The  mural  resiliency  of  a  cavity  is  also  an  important  deter- 
mining factor  in  the  character  of  the  tympanitic  sound:  in  two  cavities 
of  equal  size,  the  one  having  the  more  relaxed  walls  affords  the  lower 
pitched  and  intenser  sound.  It  is  common  to  find  a  dull  undertone 
to  the  tympany  over  a  pulmonary  cavity  adjacent  to  a  patch  of  pul- 
monary infiltration  or  of  pleural  thickening  (Fig.  83). 

Over  a  pneumothorax,  or  an  effusion  of  air  within  the  pleural 
sac,  loud  tympany,  perhaps  of  a  metallic  tone,  is  heard  on 
percussion,  provided  that  the  mural  tension  is  not  excessive.  If 
this  be  so,  the  percussion  sound,  -although  unnaturally  intense,  is 
dull  and  muffled  and  toneless.  Pneumothoracic  tympany  frequently 
extends  far  beyond  the  anterior  and  the  inferior  borders  of  the  lung, 
owing  to  the  tendency  of  the  air  to  fill  the  complementary  pleural 
sinus.  Therefore,  the  tympany  encroaches  upon  the  dull  areas 
overlying  the  heart,  the  liver,  and  the  spleen,  from  whichever  quarter 
the  effusion  spreads.  Upward  extension  of  the  hyperresonance  also 
takes  place,  for  the  lung  above  a  pneumothorax  is  relaxed  by  the 
upward  pressure  of  the  intrapleural  air:  in  the  extreme  instance  the 
entire  side  of  the  chest  emits  an  intensely  tympanitic  percussion  sound. 
Since  a  pneumothorax  eventually  excites  pleural  effusion  into  the 
air-distended  sac,  the  tympanitic  area  sooner  or  later  is  underlaid 
by  a  zone  of  flatness,  which,  unlike  the  flatness  of  a  simple  inflam- 
matory exudate,  shifts  with  the  subject's  change  of  position 
(Fig.  81). 

Parabronchial  consolidations  conduct  the  normal  percussion 
tympany  of  the  large  bronchi  and  the  trachea,  tympany  from  this 
cause  being  demonstrable  by  percussing  over  tuberculous  and  pneu- 
monic consolidations  lying  between  the  larger  bronchi  and  the  inner 
surface  of  the  thorax  (Fig.  81). 

Amphoric  Resonance. — This  is  a  variety  of  tympany  characterized 
by  a  prolonged  empty,  echoing  sound  of  high  pitch  and  distinctive 
metallic  quality.  It  may  be  fairly  well  imitated  by  flapping  the 


EXAMINATION    OF    THE    BRONCHOPULMONARY    SYSTEM      147 

cheek  with  the  finger  when  the  mouth  is  closed  and  moderately  dis- 
tended with  air,  or  by  tapping  the  side  of  an  empty  jar — hence  the 
term,  "jug  sound." 

Amphoric  resonance  may  be  demonstrated  by  forcible  percussion 
over  an  air-containing  cavity  of  fair  size  and  superficial  situation, 
with  smooth,  thin,  moderately  tense  walls,  and  a  small  outlet,  or 
none  at  all.  Pneumothorax  and  tuberculous  cavities  occasionally, 
though  by  no  means  frequently,  afford  tympany  of  this  peculiar 
echoing  character. 

Cracked-pot  Resonance. — This  form  of  tympany  is  recognized 
by  its  distinctive  chinking  quality,  which  has  been  likened  to  the 
muffled  chink  of  coins  (money-chink  resonance),  and  to  the  sound 
produced  by  striking  the  side  of  a  cracked  metal  jar  (cracked-pot 
sound ;  bruit  de  pot  }ele) .  This  sound  may  be  counterfeited  by  clasping 
the  hands  so  as  to  form  a  cavity,  and  striking  them  sharply  against 
the  knee,  thus  suddenly  expelling,  with  an  audible  "chink,"  a  jet 
of  air  through  the  constricted  orifice  between  the  opposed  palms. 
The  essential  element  of  the  cracked-pot  sound  is  the  sudden  expul- 
sion of  air  from  a  cavity  through  a  small  opening,  and  this  noise 
blends  with  the  ordinary  tympany  of  the  cavity  to  produce  the  char- 
acteristic sharp  "chink."  To  elicit  the  sign,  strong  percussion  should 
be  made  during  expiration,  the  patient's  mouth  being  open  when  the 
blow  is  struck. 

Interpreted  in  connection  with  other  physical  signs,  the  cracked- 
pot  sound  is  an  important  indication  of  a  cavity,  but  as  a  single 
isolated  finding,  it  is  of  most  uncertain  utility.  It  is  to  be  heard, 
especially  at  an  apex,  over  a  superficial  cavity  with  tense,  though 
resilient,  walls,  and  a  free  bronchial  outlet,  and  at  the  base  over 
a  pneumothorax  communicating  with  the  air  by  a  fistula  leading 
either  into  a  bronchus  or  through  the  chest- wall  (Fig.  83).  The 
sound  is  also  sometimes  elicited  over  an  acutely  congested  lung,  as 
well  as  over  the  relaxed,  compressed  pulmonary  tissue  above  the 
upper  level  of  a  pleural  effusion.  A  highly  resilient  normal  chest, 
if  percussed  with  considerable  force,  may  emit  a  spurious  cracked- 
pot  sound,  produced  by  the  rush  of  the  escaping  air  plus  the  loud 
sound  of  pulmonary  resonance.  It  is  not  uncommon  to  find  this 
in  the  young  child,  particularly  during  the  act  of  crying,  which, 
by  narrowing  the  glottis,  impedes  the  egress  of  the  air-columns 
set  in  motion  by  the  percussion  blow.  As  already  pointed  out,  a 
cracked-pot  sound  may  be  closely  imitated  should  the  pleximeter 
finger  not  be  closely  applied  to  the  surface  of  the  chest  when  the 
percussion  blow  is  delivered. 

Special  Tonal  Changes  of  the  Percussion  Sound. — Several 


148 


PHYSICAL   DIAGNOSIS 


distinctive  alterations  in  the  pitch,  intensity,  quality,  and  permanence 
of  the  percussion  sound  have  been  described  as  aids  in  determining 
not  only  the  initial  diagnosis  of  solid  and  hollow  pulmonary  lesions, 
but  also,  in  the  case  of  the  latter,  in  gaging  the  size  and  the  shape  of 
the  cavity,  the  amount  of  its  contained  fluid,  and  the  patency  of  its 
communication  with  the  external  air. 

Wintrich's  Sign, — Percussion  over  a  cavity  gives  clearer,  louder, 
and  higher  pitched  tympany  when  the  patient's  mouth  is  open  than 
when  it  is  closed.  This  change  of  note,  known  as  Wintrich's  sign, 
is  found  over  superficial  cavities  and  over  pneumothorax,  in  either 
of  which  conditions  a  free  bronchial  communication  is  essential  for 
its  production,  the  mechanism  of  which  consists  in  the  transmission 
of  the  percussion  vibrations  to  the  tracheal  air-columns,  and  thence 


Fig.  84. — Wintrich's  interrupted  change  of  note. 


to  the  mouth,  where  they  are  amplified  and  resonated  by  the  action 
of  the  pharynx.  In  eliciting  Wintrich's  change  of  note  the  examiner's 
ear  should  be  kept  directly  beneath  the  open  mouth  of  the  patient, 
who  is  instructed  to  elevate  the  chin,  to  protrude  the  tongue,  and  to 
inspire  forcibly,  even  beyond  the  ordinary  acme  of  inspiratory  excur- 
sion. The  sign  can  be  fairly  well  imitated  by  percussing  over  the 
trachea,  first  with  the  subject's  lips  tightly  closed  and  then  with  them 
wide  agape. 

If  Wintrich's  sign  appears  and  disappears,  depending  upon  the 
posture  of  the  patient's  body,  the  change  is  termed  Wintrich's  inter- 
rupted change  of  note.  This  sign  indicates  a  cavity  containing  fluid, 
which  shifts  as  the  subject  changes  his  position,  so  that  the  bronchial 
outlet  is  alternately  occluded  and  left  unobstructed  (Fig.  84). 


EXAMINATION   OF   THE    BRONCHOPULMONARY    SYSTEM 


149 


Williams'  Trachea!  Tone. — Percussion  over  an  infiltrated  or  a  com- 
pressed apical  lesion  may  show  an  alteration  of  note  similar  to  that 
of  Wintrich,  the  sound  changing  from  dulness,  when  the  patient's 
mouth  is  closed,  to  clear  high-pitched  tracheal  tympany  when  the 
mouth  is  open — the  tracheal  tone  of  Williams.  An  analogous  tonal 
alteration  has  been  found  by  Hoover  when  the  upper  part  of  the 
sternum  is  percussed  in  cases  of  anterior  mediastinal  new-growth, 
aneurism  of  the  ascending  aortic  arch,  and  large  pericardial  effusion; 
and,  according  to  Grober,  tympany  with  a  Wintrich  tone  change  is 
demonstrable  in  tumors  of  the  posterior  mediastinal  space.  The 
production  of  Williams'  tracheal  tone  in  the  foregoing  lesions  depends 


Low-pitched  tympany  with  subject  erect.  High-pitched  tympany  with  subject  recumbent 

Fig.  85. — Gerhardt's  sign. 

upon  the  transmission  of  the  percussion  waves  to  the  trachea,  whose 
air-columns,  thus  agitated,  lend  a  tracheal  quality  to  the  sound 
primarily  excited  in  the  area  percussed. 

Friedreich's  Sign. — Inspiratory  elevation  and  expiratory  lowering 
of  the  pitch  of  cavity  tympany  is  known  as  Friedreich's  sign,  which 
requires  for  its  production  physical  conditions  identical  with  those 
responsible  for  Wintrich's  change  of  note.  Respiratory  change  of 
pitch  is  attributed  to  variations  in  the  mural  tension  of  the  cavity 
and  in  the  size  of  the  chink  of  the  glottis,  which  occur  with  the  act 
of  breathing.  Unless  associated  with  other  more  definite  indications 
of  a  cavity,  Friedreich's  sign  is  likely  to  be  misleading — a  similar 
respiratory  change  of  pitch,  differing  from  it  chiefly  in  degree,  may 


PHYSICAL    DIAGNOSIS 


be  readily  demonstrated  by  vigorous  percussion  over  the  normal 
lungs,  owing  to  differences  in  pulmonary  tension  during  inspiration 
and  expiration.  (Cf.  Adherent  Pericardium.) 

Gerhardt's  Sign. — This  is  a  change  of  note  relating  to  the  shape  of 
a  pulmonary  cavity,  and  consists  of  an  alteration  in  the  pitch  of  the 
percussion  tympany,  occurring  when  the  patient's  posture  is  changed. 
In  order  to  afford  this  change  of  pitch  a  cavity  must  be  partly  filled 
with  fluid,  have  unequal  axes,  and  have  an  unobstructed  bronchial 
outlet.  Under  these  circumstances  the  pitch  of  the  tympany  is 
lower  when  the  long  axis  of  the  cavity  is  horizontal  than  when 
it  is  vertical^  (Fig.  85).  Thus,  a  cavity  with  a  long  horizontal 
axis  emits  a  lower  tympany  when  the  patient  sits  erect  than  when 
he  lies  upon  the  back,  while  one  with  a  long  vertical  axis  affords 

higher  pitched  tympany  under 
the  same  conditions  of  pos- 
ture. An  identical  change  of 
pitch,  known  as  Biermefs  sign, 
may  be  elicited  over  a  hydro- 
pneumothorax,  in  which  con- 
dition the  percussion  tympany 
is  low  pitched  when  the  patient 
is  recumbent  and  high  pitched 
when  he  is  erect,  since  in  re- 
cumbency the  long  horizontal 
axis  of  the  pleural  cavity  is 
increased  by  the  gravitation  of 
the  fluid.  Of  these  two  signs, 
Biermer's  is  the  more  constant. 
This  is  so  because  the  pleural 
cavity  more  readily  provides 
the  necessary  acoustic  condi- 
tions than  a  pulmonary  excava- 
tion— the  former  frequently  serves  as  a  simple  oval  resonating 
chamber,  while  the  latter  is  ordinarily  of  exceedingly  irregular  shape, 
with  several  axes  of  unequal  length. 

Bell  Tympany. — In  pneumothorax  a  distinctive  metallic  echo 
(bruit  d'airairi)  may  be  elicited  by  a  special  sort  of  auscultatory 
percussion  known  as  Gairdner's  coin-test  (Fig.  86).  This  consists 
of  auscultating  over  the  lower  thorax  posteriorly,  while  an  assistant 
percusses  at  the  same  level  anteriorly,  using  the  edge  of  one  large 
silver  coin  &.s  a  plexor  and  the  flat  surface  of  another  as  a  pleximeter. 
If  the  pleural  sac  be  filled  with  air,  the  impact  of  the  two  coins  is 


Fig.  86. — Mechanism  of  bell  tympany. 


EXAMINATION    OF    THE    BRONCHOPULMONARY    SYSTEM       151 

heard  as  an  echoing  metallic  ring,  not  unlike  the  distant  sound  of  a 
hammer  and  anvil  or  of  a  chime  of  bells.  It  is  also  possible  to  hear 
the  bell  sound  over  a  large,  empty,  superficial  pulmonary  cavity 
having  the  resonating  properties  of  a  pneumothorax. 

Here  may  be  mentioned  the  transmission  of  the  metallic  click  of 
two  coins,  demonstrable  by  the  above  technic  in  pleural  effusions 
(Pitres's  signe  du  sou).  This  sound,  however,  wholly  lacks  the 
chiming  tone  so  typical  of  pneumothorax,  being  harder,  more 
"chinky,"  and  less  echoing.  The  tone  is  simply  dull  when  fluid 
and  consolidation  coexist. 

The  Lung  Reflex. — Not  infrequently  a  circumscribed  area  of  pul- 
monary resonance  becomes  decidedly  hyperresonant  after  prolonged 
and  vigorous  percussion,  this  alteration  of  sound  being  ascribed  to  a 
temporary  dilatation  of  the  lung,  excited  reflexly,  beneath  the  part 
percussed.  Abrams  has  described,  under  the  term  lung  reflex,  this 
sort  of  circumscribed  hyperresonance  resulting  from  local  irritation 
of  the  surface  of  the  chest  by  the  application  of  heat,  cold,  friction, 
and  mustard,  which  apparently  provokes  dilatation  of  the  vesicular 
tissue  beneath  the  irritated  surface  area. 

AUSCULTATION  OF   THE   LUNGS 

Auscultation  is  the  means  of  studying  the  normal  respiratory 
sounds  and  their  pathologic  modifications,  of  judging  the  character  of 
the  voice  resonance,  and  of  detecting  sundry  adventitious  sounds 
produced  in  the  bronchopulmonary  structures  and  in  the  pleura. 
Either  the  mediate  or  the  immediate  method  may  be  employed, 
according  to  the  examiner's  preference — there  are  those  who  believe 
that  poorly  defined  chest  signs,  such  as  very  fine  crepitations  and 
distant  pathologic  breathing,  can  be  detected  most  easily  by  applying 
the  ear  directly  to  the  chest,  and  there  are  those  who,  accustomed  to 
using  a  stethoscope,  can  judge  respiratory  sounds  most  accurately  with 
this  instrument.  The  exceptional  instances  in  which  the  naked  ear 
serves  better  than  the  stethoscope  have  been  referred  to  in  the  pre- 
ceding section.  (See  p.  23.) 

To  obtain  trustworthy  results,  the  patient  should  breathe  regularly, 
tranquilly,  and  somewhat  more  deeply  than  normal,  thus  fully  inflat- 
ing and  deflating  the  lungs,  while  the  examiner  auscultates  systemati- 
cally over  the  different  areas  within  the  pulmonary  borders.  The 
sounds  thus  elicited  are  analyzed  and  compared  with  those  afforded 
by  deeper,  more  forcible  respiration,  which  in  some  instances  is 
necessary  to  develop  tangible  findings.  To  avoid  the  production 
of  extraneous  noises  within  the  upper  air-passages,  the  patient  is 


152 


PHYSICAL   DIAGNOSIS 


instructed  to  breathe  with  the  mouth  partly  open,  the  cheeks  and 
nares  being  relaxed,  and  to  guard  against  forcible,  noisy  respiration. 
These  essential  precautions,  though  of  themselves  simple,  are  not 
easy  to  put  in  force,  for  the  average  subject  is  not  readily  taught 
how  to  breathe  properly. 

THE    RESPIRATORY   SOUNDS 

The  respiratory  sounds  audible  over  the  normal  thorax  conform 
to  two  principal  types,  vesicular  and  bronchial,  to  which  may  be 
added,  for  convenience  sake,  a  subsidiary  variety,  which  combines 
the  characteristics  of  both,  the  bronchovesicidar .  Each  of  these 
types  of  breathing  is  audible,  in  health,  only  in  certain  definite 
regions  of  the  chest,  and,  this  being  so,  the  substitution  of  one 


Normal. 


Puerile. 


Senile. 


Harsh. 


Expiration 


Inspiration. 


Bronchial.  Bronchovesicular.  Wavy.  Cog-wheel. 

Fig.  87. — Normal  and  pathologic  types  of  the  respiratory  murmur. 

respiratory  type  by  another  (such  as  the  existence  of  bronchial  or 
of  bronchovesicular  breathing  in  a  region  normally  affording  a  pure 
vesicular  sound)  is  to  be  regarded  as  pathologic. 

Vesicular  Breathing. — The  normal  vesicular  murmur  is  a  soft, 
rustling,  breezy,  low-pitched  sound,  whose  inspiratory  and  expira- 
tory cycles  blend  so  imperceptibly  that  no  distinct  interval  of  silence 
separates  them  (Fig.  87).  The  inspiratory  phase  best  illustrates  the 
distinctive  breeziness,  the  low  pitch,  and  the  moderate  intensity  of  the 
sound,  for  during  the  expiratory  phase  the  quality  is  a  trifle  harder 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM       153 

and  more  blowing,  the  pitch  higher,1  and  the  intensity  decidedly 
less — in  fact,  the  expiratory  sound  may  be  so  weakened  that  it  is  prac- 
tically inaudible.  The  ratio  of  the  inspiratory  to  the  expiratory  sound 
is  3:1.  Normal  vesicular  breathing  may  be  imitated  with  toler- 
able accuracy  by  breathing  naturally  with  the  lips  held  in  the  position 
of  pronouncing  the  letter/.  It  may  be  heard  in  its  typical  character 
over  the  left  infraclavicular,  the  infrascapular,  and  the  axillary  regions, 
where  only  alveolar  tissue  lies  directly  beneath  the  auscultator's  ear. 

To  account  for  the  origin  of  the  vesicular  murmur  several  theories 
have  been  suggested,  no  one  of  which  appears  to  be  wholly  adequate. 
Baas'  theory  assumes  that  the  sound  is  merely  a  modification  of  the 
blowing  sounds  of  the  larynx  and  the  trachea,  which  become  softened, 
muffled,  and  otherwise  altered  by  their  conduction  through  the 
bronchopulmonary  structures.  But,  according  to  Sahli,  the  local 
movements  of  the  pulmonary  parenchyma  also  account  for  certain 
elements  of  the  vesicular  sound.  Together,  these  two  hypotheses 
serve  as  a  better  explanation  than  the  original  theory  of  Laennec, 
that  the  sound  was  due  to  the  friction  of  the  air-currents  in  the  bron- 
chioles and  the  infundibula,  or  than  Bueri's  hypothesis  of  the  im- 
pact of  central  and  peripheral  air-columns. 

Bronchial  Breathing. — Bronchial  breathing  is  distinguished  by 
its  loud,  blowing,  tubular  quality,  high  pitch,  and  the  distinct  interval 
of  silence  which  separates  inspiration  and  expiration  (Fig.  87).  Of 
the  two  breath-sounds,  expiration  is  generally  more  intense,  higher 
pitched,  and  more  distinctively  tubular.  The  duration  of  the  respira- 
tory phases  is  about  equal,  if,  indeed,  expiration  is  not  decidedly  the 
longer,  and  neither  carries  even  the  faintest  trace  of  that  soft,  quiet 
breeziness  peculiar  to  the  normal  vesicular  murmur.  The  bronchial 
respiratory  sound  may  be  elicited  in  the  healthy  adult  by  ausculta- 
tion in  those  areas  of  the  thorax  lying  directly  over  the  larynx  and 
the  trachea — the  suprasternal  notch,  the  upper  sternal  region,  and 
the  lower  cervical  vertebrae.  As  Barach  points  out,  both  bronchia] 
respiration  and  bronchophony  are  audible  at  the  acromial  end  of 
the  clavicles,  owing  to  the  excellent  conducting  properties  of 
these  bones.  The  bronchial  tone  may  be  counterfeited  by  breath- 
ing deeply  with  the  mouth  fixed,  so  as  to  pronounce  the  syllable 
"hu"  or  the  consonant  "ch." 

Bronchial  breathing  is  merely  the  unmodified  sound  of  the  laryn- 
gotracheal  murmur,  which  is  a  glottidean  tone  due  to  the  passage 
of  air-columns,  during  inspiration  and  expiration,  through  the  glottis 

1  The  truth  of  this  statement,  originally  made  by  Austin  Flint,  in  1852,  must 
be  apparent  to  one  that  judges  sound  by  intelligent  auscultation,  despite  the 
view  expressed  by  some  that  the  pitch  of  expiration  is  lower  than  that  of  inspira- 
tion. 


I$4  PHYSICAL   DIAGNOSIS 

into  the  wider  caliber  of  the  windpipe  above  and  below,  with  the 
consequent  production  of  air-eddies  and  their  reflection  both  up- 
ward toward  the  pharynx  and  downward  through  the  trachea  and 
the  larger  bronchial  tubes. 

The  detection  of  bronchial  breathing  over  areas  of  the  lung  to 
which  this  sound  is  foreign  signifies  that  in  such  areas  the  vesicular 
structure  is  in  a  condition  of  infiltration,  compression,  or  excavation, 
in  consequence  of  which  the  bronchial  tone,  normally  enfeebled  by 
healthy  pulmonary  tissue,  is  conducted  to  the  surface  of  the  chest 
with  unimpaired  intensity  and  quality.  This  type  of  respiration, 
therefore,  is  met  with  in  pneumonic  and  tuberculous  consolidations; 
in  pulmonary  and  bronchiectatic  cavities  with  a  free  bronchial  out- 
let; and  in  pulmonary  compression  and  collapse  secondary  to  pleural 
effusion,  neoplasm,  and  aneurism.  (See  Figs.  81  and  83.)  Other 
conditions  that  account  for  bronchial  respiration  are  edema,  abscess, 
gangrene,  infarction,  cirrhosis,  syphilis,  cancer,  and  actinomycosis. 
A  mass  of  enlarged  bronchial  glands  or  a  mediastinal  neoplasm 
situated  in  intimate  relation  with  the  larger  air-tubes  and  the  thoracic 
parietes  may  distinctly  transmit  to  the  latter  the  bronchial  tone. 

Full  respirations  are  essential  to  bring  out  all  the  characteristics 
of  bronchial  breathing,  as  can  be  demonstrated  by  auscultating 
over  a  consolidation,  while  the  subject  takes  alternately  shallow 
and  deep  breaths. 

Cavernous  and  amphoric  breathing  are  two  subvarieties  of 
bronchial  respiration,  distinguished  by  certain  peculiarities  in  their 
quality  and  pitch.  Cavernous  breathing  is  distinguished  by  its  deep 
and  hollow  quality,  low  pitch,  and  usually,  but  not  invariably,  by 
the  fact  that  expiration  is  of  lower  pitch  than  inspiration.  A  super- 
ficial cavity  with  resilient  walls  and  a  patent  bronchial  outlet  is  the 
usual  factor  of  this  sort  of  breathing,  such  a  cavity  being  either 
pulmonary  or  bronchiectatic,  and  due  to  tuberculosis,  abscess,  or 
gangrene.  The  proximity  of  an  area  of  infiltration  to  the  excavat:on 
may  add  to  the  cavernous  tone  a  high-pitched  tubular  bronchial 
quality  during  expiration,  and  to  this  modification  Flint  has  applied 
the  term  bronchocavernous  respiration.  A  patch  of  healthy  lung 
surrounding  a  cavity  may  ingraft  its  vesicular  quality  upon  the 
cavernous  sound,  and  thus  produce  a  hybrid  type  of  breathing  known 
as  vesiculocavernous.  The  distinctions  between  these  two  sub- 
varieties  of  cavernous  breathing,  though  hypothetically  plausible, 
are  too  finely  drawn  to  be  appreciated  save  by  one  who  possesses  a 
most  cultivated  sense  of  acoustics. 

Amphoric  breathing  is  recognized  by  its  characteristic  musical, 
metallic,  echoing  quality,  which  replaces  the  hollow  tone  of  pure 


EXAMINATION   OF    THE    BRONCHOPULMONARY    SYSTEM       155 

cavernous  and  the  tubular  blowing  of  typical  bronchial  respiration. 
The  sound  produced  by  blowing  gently  into  the  mouth  of  an  empty 
vessel  closely  imitates  the  musical  quality  of  amphoric  breathing, 
which  is  the  auscultatory  complement  of  the  amphoric  percussion- 
note  and  of  the  bell-tympany  elicited  over  pneumothoracic  and 
large  pulmonary  cavities.  The  pitch  of  the  foregoing  types  of  breath- 
ing depends  chiefly  upon  the  size  of  the  cavity,  being  higher  the 
smaller  the  size  of  the  resonating  chamber,  and  vice  versa. 

A  minor  subvariety  of  bronchial  breathing,  known  as  Seitz  meta- 
morphosing respiration,  is  distinguished  by  an  inspiratory  murmur 
beginning  as  a  tubular  bronchial  sound,  and  ending  as  either  a  caver- 
nous or  an  amphoric  tone.  Less  commonly,  this  change  of  quality 
affects  expiration  or  both  respiratory  phases.  This  bronchocaver- 
nous  breath-sound  is  afforded  by  a  cavity  having  a  small  patent 
bronchial  outlet.  Over  tuberculous  infiltrations  there  is  sometimes 
to  be  heard  a  type  of  breathing  beginning  as  a  vesicular  and  ending 
as  a  bronchial  or  bronchovesicular  sound — the  "veiled  puff"  ("souffle 
mold"}  of  Laennec. 

Bronchovesicular  Breathing. — This  type  of  respiration,  as  its 
name  suggests,  is  a  mixture  of  the  bronchial  and  vesicular  murmurs, 
such  as  may  be  heard  in  those  areas  of  the  normal  thorax  where  the 
range  of  auscultation  includes  the  sounds  of  both  the  large  bronchi 
and  the  vesicular  structure.  It  is  audible,  therefore,  over  and  along- 
side the  sternum  at  the  level  of  Louis'  angle,  and  over  the  inter- 
scapular  spaces  on  each  side  of  the  spine,  at  the  level  of  the  third  or 
fourth  thoracic  vertebra,  these  being  the  situations  where  the  primary 
bronchi,  covered  by  an  intervening  layer  of  vesicular  tissue,  lie  close 
to  the  surface  of  the  chest.  The  sound  is  louder  and  decidedly  more 
bronchial  in  tone  on  the  right  side,  owing  to  the  anatomic  peculiarities 
of  the  right  bronchus. 

The  inspiratory  phase  of  bronchovesicular  breathing  is  purely 
vesicular,  or,  less  commonly,  tinged  with  a  bronchial  tone,  while 
expiration  is  of  a  more  bronchial  character.  Expiration  is  as 
long  as,  if  not  longer  than,  inspiration,  which,  aside  from  its 
shorter  duration,  is  the  quieter  and  the  lower  pitched  of  the  two 
sounds.  No  matter  what  be  its  finer  acoustic  variations, — and  their 
number  is  legion, — so  long  as  respiration  affords  this  blending  of  the 
bronchial  and  vesicular  sounds,  the  term  bronchovesicular  is  applic- 
able, or,  if  one  chooses,  a  synonymous  adjective  like  rude,  sub- 
tubular,  indeterminate,  or  transition  (Fig.  87). 

Pathologically,  bronchovesicular  breathing  occurs  as  the  result 
of  pulmonary  lesions  that  conduct  the  bronchial  tone  to  the  surface 
of  the  chest,  along  with  more  or  less  of  the  normal  vesicular  murmur 


156  PHYSICAL   DIAGNOSIS 

(Fig.  81).  This  acoustic  condition  is  fulfilled  by  small,  disseminated 
consolidations  separated  by  unimplicated  vesicular  structure,  as  in 
catarrhal  pneumonia  and  incipient  phthisis;  by  a  large  area  of  con- 
solidation or  excavation  adjacent  to  healthy  lung,  as  in  central  crou- 
pous  pneumonia,  tuberculous  infiltration,  and  pulmonary  or  bronchi- 
ectatic  cavities  overlaid  by  normal  pulmonary  tissue;  by  an  area  of 
compressed,  atelectatic  lung,  such  as  the  zone  of  pressure  atelectasis 
lying  directly  above  a  pleural  effusion.  The  bronchial  element  of 
bronchovesicular  breathing  may  diminish  or  disappear,  should  the 
bronchial  tube  communicating  with  the  infiltrated  or  excavated  patch 
be  obstructed  by  secretion,  while  the  vesicular  element  may  be 
similarly  modified,  should  the  tube  leading  to  the  healthy  vesicular 
area  be  blocked.  Bronchovesicular  respiration  is  especially  signifi- 
cant of  some  pathologic  factor  when  it  is  elicited  over  parts  of  the 
lungs  well  removed  from  the  normal  sites  of  this  type  of  breathing, 
but  these  areas  are  by  no  means  exempt  from  consolidative  processes. 

Prolonged  Harsh  Expiration. — Reversal  of  the  inspiratory- 
expiratory  ratio,  with  harshness  and  impurity  of  the  expiratory 
sound,  denotes  some  impediment  to  the  free  egress  of  the  broncho- 
pulmonary  air-columns  during  the  act  of  breathing,  and,  in  general 
terms,  it  may  be  stated  that  the  greater  this  interference,  the  more 
decided  the  impurity  and  the  lengthening  of  the  sound  (Fig.  87). 
At  the  left  apex  prolonged  high-pitched  expiration  is  exceedingly 
suggestive  of  tuberculous  infiltration,  while  a  prolonged  low-pitched 
expiratory  sound,  audible  over  the  greater  part  of  both  lungs,  is 
found  in  the  chronic  bronchitides  of  emphysema  and  asthma. 
Undue  prolongation  and  harshness  of  the  expiratory  murmur  is  to 
be  expected  as  a  physiologic  sign  over  the  upper  part  of  the  right 
lung. 

Puerile  or  Exaggerated  Breathing. — An  exaggeration  in  the 
intensity  of  the  vesicular  murmur  is  known  as  exaggerated,  harsh, 
rough,  or  puerile  breathing.  This  type  of  respiration  is  physiologic 
in  children  below  the  age  of  puberty,  being  more  pronounced  the 
younger  the  child;  in  the  healthy  adult  it  is  audible  above  and  below 
the  right  clavicle,  and  frequently  also  at  the  left  base  posteriorly 
(Cabot) .  A  thin,  elastic  chest- wall  magnifies  the  vesicular  murmur, 
perhaps  to  the  degree  of  puerility,  while  a  thick,  rigid  chest  blocks 
the  transmission  of  the  sound. 

Pathologically,  puerile  breathing  is  elicited  over  a  lung  that  is 
variously  overacting  in  consequence  of  crippling  of  the  opposite 
lung  by  a  wide-spread  congestion,  infiltration,  effusion,  or  neoplasm; 
or  over  a  circumscribed  portion  of  a  lung  that  is  overworked,  so  as 
to  compensate  for  a  lesion  elsewhere  in  the  same  lung.  Catarrhal 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM       157 

obstruction  of  the  smaller  bronchi  is  a  most  important  cause  of  harsh, 
rough  breathing,  owing  to  the  stenotic  interference  with  the  move- 
ments of  the  bronchiolar  air-columns  attending  this  affection.  Dysp- 
neic  overaction  of  the  lungs,  such  as  that  incident  to  active  muscular 
exertion  or  to  uncompensated  cardiac  disease,  may  also  account 
for  abnormal  intensity  and  harshness  of  the  breath-sounds. 

Puerile  and  bronchovesicular  breathing  are,  superficially,  not 
unlike,  but  they  differ  in  that  the  former,  though  loud  and  harsh,  is 
untainted  by  the  bronchial  tubular  tone  and  is  not  attended  by  any 
disturbance  in  the  normal  inspiratory-expiratory  ratio.  These  dif- 
ferences also  serve  to  differentiate  bronchial  breathing,  should  it 
prove  a  source  of  confusion. 

Senile  or  Feeble  Breathing  (Fig.  87). — Enfeeblement  of  the  vesic- 
ular murmur,  or  senile  breathing,  is  common  in  the  aged  and  in  states 
of  asthenia  and  debility,  as  the  result  of  defective  pulmonary  resiliency 
and  of  weak  respiratory  movements.  Normal  lungs  may  emit 
suppressed,  distant  sounds  simply  because  the  subject  breathes  so 
quietly  that  the  vesicles  are  improperly  inflated  with  inspiration. 

In  disease  a  senile  type  of  breathing  is  symptomatic  of  many  differ- 
ent conditions  relating  to  defective  distention  of  the  pulmonary 
alveoli  and  to  the  non-conduction  of  the  normal  pulmonary  murmur. 
In  paralysis  of  the  respiratory  muscles  and  in  painful  affections,  such 
as  acute  pleurisy,  pleurodynia,  and  trauma  of  the  chest,  it  is  natural  to 
expect  suppressed,  quiet  breathing,  because  of  the  limited  thoracic 
expansion.  In  bronchial  obstruction,  as  by  foreign  body,  pressure, 
or  secretion,  diminution  of  the  respiratory  murmur  is  elicited  over  that 
part  of  the  pulmonary  parenchyma  supplied  by  the  stenotic  tube,  the 
general  rule  holding  true  that  the  higher  the  location  of  the  obstruc- 
tion, the  larger  the  area  of  enfeebled  sound.  Imperfect  vesicular 
distention,  weakening  the  breath-sounds,  may  occur  in  chronic  adhe- 
sive pleurisy,  owing  to  restriction  of  the  pulmonary  excursions  by 
dense  fibrous  bands;  in  hypertrophic  emphysema,  because  of  the 
rigid,  overinflated  condition  of  the  vesicles;  in  the  first  stage  of 
croupous  pneumonia,  when  the  lungs  are  engorged  and  fixed  and 
abnormally  tense;  in  atelectasis  (due  to  either  obstruction  or  com- 
pression) for  the  reason  that  the  affected  area  receives  no  air  supply 
and  is  too  relaxed  to  vibrate.  In  disseminated  tuberculous  infiltra- 
tion the  respiratory  sounds  may  be  weakened  as  the  result  of  hyper- 
tension of  the  non-tuberculous  portions  of  the  lungs  and  from  cir- 
cumscribed catarrhal  stenosis  of  the  small  bronchi  (Sahli),  though 
more  commonly  this  type  of  infiltration  is  betrayed  by  broncho- 
vesicular  or  by  harsh,  impure  breathing.  The  respiratory  sounds  are 


1 58  PHYSICAL   DIAGNOSIS 

suppressed  in  some  cases  of  active  congestion,  edema,  and  cirrhosis 
of  the  lungs,  and  in  those  forms  of  massive  pneumonia  in  which 
a  fibrinous  exudate  blocks  a  large  part  of  the  bronchial  lumen. 

Enfeeblement  of  the  respiratory  sounds,  by  fault  of  their  poor 
conduction  to  the  surface,  is  found  when  a  liquid  or  a  solid  media  is 
interposed  between  the  lungs  and  the  chest-wall.  The  sound  is 
damped  in  this  manner  by  extensive  pleural  effusions,  by  pleural 
thickening,  and  by  intrathoracic  new-growths  not  continuous  with  the 
pleuropulmonary  surfaces.  In  pneumothorax  the  breath-sounds 
become  weak  and  indistinct  when  the  bronchial  outlet  of  the  cavity 
is  obstructed. 

Absent  Breathing. — Total  suppression  of  the  respiratory  murmur 
occurs  as  the  result  of  any  change  acting  as  an  effectual  barrier  to 
the  conduction  of  bronchopulmonary  sounds  to  the  surface  of  the 
chest.  Any  factor  of  senile  breathing,  therefore,  may  altogether  sup- 
press the  breath-sounds,  should  it  produce  the  essential  acoustic 
conditions  of  such  a  change.  The  most  important  causes  of  totally 
absent  breath-sounds  are  pleural  exudates  and  transudates,  bronchial 
and  bronchiolar  obstruction,  closed  pneumothorax,  and  pulmonary 
cavities  filled  with  liquid — conditions  which,  it  is  obvious,  may 
block  all  sound  vibrations  at  some  point  between  their  origin  in  the 
glottis  and  the  surface  of  the  thorax  (Fig.  81). 

Cog-wheel  or  Interrupted  Breathing. — In  this  type  of  breathing 
the  inspiratory  murmur  is  interrupted  by  a  series  of  short,  jerky 
pauses,  or  it  is  composed  of  a  succession  of  undulatory,  wavy  sound 
modulations;  less  commonly  these  peculiarities  are  audible  during 
expiration.  More  or  less  exaggeration  and  impurity  of  the  whole 
vesicular  murmur  frequently  accompanies  the  foregoing  changes 
although  they  may  also  be  attended  by  suppression  of  the  breath- 
sounds  (Fig.  87). 

Circumscribed  cog-wheel  breathing  indicates  catarrh  of  the  finer 
bronchi,  with  obstruction  to  the  free  movements  of  the  bronchiolar 
air-columns  and  irregular  inflation  and  deflation  of  the  lobules 
supplied  by  the  inflamed  tubes.  This  change  is  commonly  found 
in  early  phthisis,  of  which  cog-wheel  respiration  (especially  if  localized 
at  the  apex)  is  a  most  suggestive  physical  sign.  Generalized  cog-wheel 
breathing  over  the  whole  thorax  is  due  simply  to  intermittent  con- 
tractions of  the  respiratory  muscles,  and  it  means,  therefore,  nothing 
more  serious  than  fatigue,  nervousness,  chest  pain,  or  perhaps  incom- 
plete paralysis  of  the  muscles  concerned  in  breathing. 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM       159 


VOCAL    RESONANCE 

Vocal  or  voice  resonance,  which  bears  the  same  relation  to  auscul- 
tation as  does  vocal  fremitus  to  palpation,  has  the  same  physical 
origin  as  its  tactile  equivalent,  and  is  modified  by  pathologic  proc- 
esses identical  with  those  that  influence  the  latter.  The  audible 
and  tactile  fremitus,  then,  correspond,  under  both  normal  and  abnormal 
conditions,  and  hence  are  corroborative  in  the  study  of  the  laryngo- 
tracheal  voice  vibrations  by  the  senses  of  touch  and  of  hearing. 

In  eliciting  vocal  resonance  the  stethoscope  should  be  placed  over 
a  region  of  the  chest  not  immediately  adjacent  to  the  main  bronchial 
tree,  while  the  patient  repeats  " ninety-nine"  or  "one,  two,  three," 
with  his  lips  turned  away  from  the  auscultator's  ear.  Normal 
vocal  resonance  sounds  like  a  confused,  buzzing  hum  that  carries 
no  trace  of  articulate  sound — it  is  merely  an  indistinct,  far-away 
vibration,  which  seemingly  arises  within  the  depths  of  the  thorax, 
and  never  conveys  to  the  examiner  the  clean-cut,  sharp  pronuncia- 
tion of  the  words  uttered  by  the  speaker.  Auscultation  just  above 
the  lower  pulmonary  borders  typically  illustrates  these  peculiarities 
of  the  sound.  The  resonance  of  the  voice,  like  its  fremitus,  is  normally 
exaggerated  over  the  site  of  the  large  air-passages,  and  is  modified 
by  the  pitch  and  intensity  of  the  subject's  voice  and  by  the  conducting 
qualities  of  the  thoracic  parietes. 

Increased  Vocal  Resonance. — As  a  pathologic  change,  increase 
in  the  intensity  of  the  voice  resonance  depends  upon  pulmonary 
infiltration,  excavation,  or  compression,  and  upon  bronchiectatic 
cavities,  the  several  underlying  causes  of  which  have  already  been 
enumerated  (Fig.  81).  Bronchophony,  or  the  bronchial  voice,  is 
the  term  used  to  express  an  exaggeration  of  vocal  resonance  so 
striking  that  it  seems  as  if  it  were  produced  just  beneath  the  chest- 
wall,  though,  in  spite  of  its  intensity,  bronchophony  invariably  remains 
a  confused,  inarticulate  rumble.  Normally,  this  bronchial  sound 
is  audible  over  the  course  of  the  trachea  and  primary  bronchi.  Pec- 
toriloquy,  a  refinement  of  ibronchophony,  is  the  transmission  of 
articulate  speech  to  the  surface  of  the  thorax,  where  not  only  the  spoken 
words,  but  also  their  syllables,  are  heard  with  a  clear,  distinct  inten- 
sity. Whispering  pectoriloquy,  or  the  conduction  of  the  articulate 
whisper  through  the  chest-wall,  is  a  still  greater  refinement  of  bron- 
chophony, and  stands  for  the  acme  of  increased  vocal  resonance, 
in  which  the  sound  conduction  is  exquisitely  developed.  Pectoriloquy, 
either  spoken  or  whispering,  is  most  suggestive  of  a  cavity,  but  it  is 
not  restricted  to  such  a  lesion,  as  Laennec  believed,  since  it  is  not 


l6o  PHYSICAL   DIAGNOSIS 

infrequently  audible  over  an  area  of  pulmonary  infiltration  or  com- 
pression. Page  proposes  the  word  bronchiloquy  to  express  the  high- 
pitched  pectoriloquy  due  to  a  consolidated  lung,  and  the  term  cavern- 
iloquy,  for  the  low-pitched  pectoriloquy  afforded  by  a  cavity,  while 
he  designates  as  amphoriloquy  the  intense  amphoric  voice-sounds 
which  correspond  to  the  amphoric  percussion-note  and  respiration. 
Egophony  is  a  form  of  bronchophony  characterized  by  a  peculiar 
quavering  nasal  tone,  comparable  to  the  bleating  of  a  goat.  This 
sign,  whose  mechanism  is  not  understood,  is  sometimes  heard  just 
above  the  upper  level  of  a  pleural  effusion,  and  also  above  various 
pulmonary  infiltrations.  Its  clinical  significance  does  not  differ  from 
that  of  the  ordinary  bronchial  voice. 

Baccellfs  sign,  or  the  transmission  of  whispering  pectoriloquy 
through  a  serous,  but  not  through  a  purulent,  pleural  effusion  has 
been  used  as  a  point  of  differentiation  between  these  two  conditions, 
but  on  insufficient  grounds,  for  though  absent  over  an  empyema, 
the  whispered  voice  is  also  inaudible  over  many  serous  effusions  of 
large  volume. 

Decreased  Vocal  Resonance. — Enfeebled,  sometimes  absent,  voice 
resonance  is  to  be  expected  as  the  result  of  emphysema,  bronchial 
occlusion,  thickened  pleura,  pleural  effusions,  and  the  other  causes 
of  diminished  tactile  fremitus  referred  to  in  a  preceding  section. 
(See  p.  133.) 

ADVENTITIOUS    SOUNDS 

In  addition  to  the  several  modifications  of  the  vesicular  murmur  just 
described,  certain  superadded,  foreign  sounds  arise  in  consequence 
of  pathologic  changes  affecting  the  bronchial  tubes,  the  pulmonary 
parenchyma,  and  the  pleura  (Fig.  88).  The  following  classification 
of  these  abnormal  or  adventitious  sounds  is  sufficient  for  clinical 
purposes : 

RALES. 

j~.     .  /  Sibilant.  Small  bronchi. 

\  Sonorous.  Large  bronchi;  trachea. 

(  Crepitant.  Air- vesicles;  infundibula. 
Moist  :<  Subcrepitant.        Bronchioles. 

(Mucous.  Bronchi;  trachea;  cavities. 

PLEURAL  FRICTION.  Pleural  surfaces. 
SPLASHING  SOUNDS. 

Succussion  sounds.  Pleural  or  pulmonary  cavity. 

Metallic  tinkle.  Pleural  or  pulmonary  cavity. 


EXAMINATION   OF   THE   BRONCHOPULMONARY   SYSTEM      l6l 

Extraneous  sounds  produced  upon  the  surface  of  the  body  may 
prove  sources  of  error  in  diagnosis,  from  their  resemblance  to 
intrathoracic  adventitious  sounds,  such  as  harsh  breathing,  rales, 
and  friction.  Of  these  extraneous  noises,  perhaps  the  commonest 
are  the  so-called  muscle  sounds,  which  are  comparable  to  a  series 
of  low,  distant,  muffled  rumbles  or  to  an  interrupted  humming, 
audible  during  both  the  active  and  the  quiescent  stages  of  breath- 
ing. Those  heard  during  active  respiration  are  generally  attribu- 
table to  the  movements  of  the  thoracic  musculature  or  to  friction 
between  the  patient's  skin  and  the  stethoscope;  they  naturally 


Moist  rales. 


Dry  rales. 


Fig.  88. — Mechanism  of  rales. 

disappear  when  the  patient  stops  breathing.  Those  heard  when 
the  subject's  chest  is  motionless  are  usually  referable  to  fibrillary 
muscular  contractions  or  to  pressure  upon  muscular  bundles  by  the 
chest-piece  of  the  stethoscope;  they  cease  when  the  latter  is  applied 
gently  and  evenly,  and  when  immediate  is  substituted  for  instru- 
mental auscultation.  Crackling  sounds,  due  to  the  application  of 
the  stethoscope  to  a  dry,  hairy  surface  (hair  crepitus),  may  remind 
one  of  crepitant  rales;  but  these  false  crepitations  are  equally  loud 
and  clear  with  both  inspiration  and  expiration,  may  be  produced 
at  will  by  the  improper  adjustment  of  the  stethoscope,  and  disappear 


1 62  PHYSICAL   DIAGNOSIS 

when  the  hairy  part  is  moistened  before  the  chest-piece  is  pressed 
against  it. 

Rales. — In  a  clinical  sense  the  term  rale  includes  those  adventi- 
tious vibratory  noises  due  to  interference  with  the  free  movements 
of  the  air  within  the  bronchopulmonary  structures  by  the  presence 
of  fluid  or  by  a  constriction  of  the  bronchial  lumen.  According  to 
the  absence  or  the  presence  of  liquid  at  their  site  of  origin,  rales  are 
classed  as  either  dry  or  moist;  and  according  to  their  anatomic  seat 
of  production,  as  bronchial,  vesicular,  and  cavernous;  or,  should  they 
originate  in  the  upper  air-passages,  as  bticcal,  laryngeal,  and  tracheal. 

In  general,  it  may  be  said  of  bronchopulmonary  rales  that  they 
convey  to  the  examiner  the  impression  of  arising  deep  within  the  lungs, 
that  they  are  likely  to  be  disseminated  as  well  as  circumscribed,  that 
they  are  prone  to  disappear,  to<reappear,  and  to  alter  their  situation 
as  the  result  of  deep  inspiration  and  coughing,  and  that  their  char- 
acteristics are  unaltered  by  external  pressure  over  their  site.  Further- 
more, as  Ransom  has  pointed  out,  some  individuals  suffering  from 
bronchial  catarrh  whose  chests  are  quite  free  from  adventitious  sounds 
so  long  as  they  stand  upright,  show  abundant  rales  directly 
they  assume  the  lateral  decubitus. 

Dry  Rales. — These  are  dry,  snoring,  whistling,  or  musical  sounds 
of  variable  pitch,  intensity,  and  quality,  arising  within  the  bronchi 
and  the  larger  air-passages  as  the  result  of  constriction  of  their 
lumen,  due  commonly  to  a  turgescent  mucosa,  to  spasmodic  con- 
traction of  the  muscularis,  to  mechanical  obstruction  by  masses  of 
viscid,  tenacious  secretion,  and,  rarely,  to  extrabronchial  pressure.1 
In  the  tubes  thus  narrowed  the  air-columns,  as  they  rush  past  the 
barrier  into  the  wider  lumen  beyond,  set  up  vibrations  recognizable 
by  the  ear  as  rales,  and  by  the  hand  as  rhonchal  fremitus  (Fig.  88). 

It  is  convenient  to  classify  dry  rales,  according  to  their  acoustic 
properties,  into  two  general  groups — sonorous  and  sibilant.  Sonorous 
rales  are  coarse,  loud,  low-pitched,  snoring  sounds  arising  within  the 
large  and  the  medium-sized  tubes,  while  sibilant  rales  are  distinguished 
by  a  shrill,  high-pitched  quality  or  by  a  soft,  cooing  tone,  and,  as  a 
rule,  are  produced  within  the  smaller  bronchi.  Exceptionally, 
however,  sibilant  sounds  may  originate  within  the  medium-sized 
tubes,  should  their  caliber  be  greatly  narrowed. 

The  sudden  and  forcible  rupture,  by  the  air-current,  of  delicate 
threads  of  mucus  stretching  across  the  bronchial  lumen  may  account 
for  the  production  of  dry  rales  endowed  with  a  peculiar  snappy, 

1  The  word  rhonchus  (L.,  rhonckus,  a  snoring  or  snorting)  is  frequently  used 
as  a  synonym  for  the  term  dry  rale,  particularly  by  English  writers. 


EXAMINATION   OF  THE   BRONCHOPULMONARY   SYSTEM      163 

crackling  quality,  while  the  simple  vibrations  of  similar  mucous 
threads  may  cause  rhonchi  having  a  musical  quality.  The  vibrations 
of  a  loosened  bit  of  bronchial  membrane  produce  a  peculiar  "flap- 
ping" rale  of  exceedingly  dry  quality,  termed  the  "bruit  de  drapeau." 
(See  Fibrinous  Bronchitis,  p.  176.)  In  interstitial  emphysema  coarse 
crepitations  and  sounds  like  small  mucous  rales  have  been  noted, 
as  the  result  of  the  action  of  the  respiratory  movements  upon  the 
bubbles  of  air  imprisoned  in  the  interalveolar  walls.  This  so-called 
emphysematous  crackling  is  very  like  the  sound  of  the  precordial 
emphysematous  murmur,  but  the  former  corresponds  to  the  respira- 
tory excursion  and  the  latter  to  the  heart-beats.  Interalveolar 
crackling  differs  from  intra-alveolar  crepitation  in  being  coarser, 
drier,  and  unrestricted  to  the  latter  part  of  the  inspiratory  cycle  of 
breathing. 

Moist  Rales. — These  are  the  various  moist,  crackling,  bubbling, 
or  gurgling  sounds,  produced  in  the  air-tubes  and  in  the  pulmonary 
parenchyma  by  the  movement  of  air  through  collections  of  fluid 
or  by  the  separation  of  agglutinated  vesicular  and  infundibular 
walls.  Such  sounds,  which  have  a  distinctively  moist  or  sticky 
quality,  may  be  classified,  according  to  their  size,  as  crepitant,  sub- 
crepitant,  and  mucous  (Fig.  88). 

Crepitant  Rales. — Crepitant  or  vesicular  rales  are  due  to  the  forcible 
separation  of  the  vesicular  and  infundibular  walls  by  the  inspiratory 
air-columns.  When  these  parts,  glued  together  by  a  viscid  or  fluid 
secretion  during  their  expiratory  deflation,  are  forcibly  separated  by 
their  inspiratory  inflation,  a  series  of  exceedingly  delicate  crackling 
sounds  is  produced,  the  quality  of  which  depends  largely  upon  the 
density  of  the  agglutinating  material,  viscid  mucus  affording  a  sticky 
sound  and  thin  fluid  a  correspondingly  liquid  sound.  The  theory  that 
the  crepitant  rale  is  really  a  form  of  pleural  friction  and  not  a  vesicular 
sound  at  all,  fails  to  carry  conviction,  and  the  weight  of  opinion  is 
strongly  against  the  intrapleural  origin  of  the  sound.  Owing  to 
the  mechanism  of  their  production,  it  is  obvious  that  crepitant  rales 
occur  during  the  latter  part  of  inspiration,  at  which  time  full  inflation 
of  the  vesicles  occurs,  with  a  consequent  tearing  apart  of  the  adherent 
mucosa;1  and,  since  all  the  agglutinated  vesicles  do  not  inflate  simul- 
taneously, these  rales  are  audible  not  as  a  single,  isolated  sound,  but 
as  a  succession  of  crepitations  or  a  shower  of  rales.  The  crepitant 

1  Very  exceptionally,  crepitations  are  audible  during  expiration,  as  in  certain 
lobular  infiltrations,  in  which,  by  fault  of  an  impermeable  bronchiolar  obstruc- 
tion, the  expiratory  air-columns  may  be  forced  backward  from  a  patch  of  healthy 
lung  into  a  collection  of  catarrhal  alveoli  whose  agglutinated  walls  are  thereby 
distended  with  distinct  crepitation. 


164  PHYSICAL   DIAGNOSIS 

rale  may  be  tolerably  well  imitated  by  rolling  a  lock  of  hair  between 
the  thumb  and  fingers  held  close  to  the  ear,  or  by  throwing  a  pinch 
of  salt  upon  a  hot  stove. 

Crepitant  rales  are  audible  in  croupous  pneumonia  during  the  stage 
of  engorgement  (crepitus  indux)  and  during  the  stage  of  resolution 
(crepitus  redux),  at  which  periods  of  the  disease  the  pulmonary 
vesicles  are  partly  filled  with  an  exudate.  Vesicular  crepitations 
are  also  heard  in  catarrhal  pneumonia,  in  tuberculous  infiltration, 
and  in  the  early  stages  of  pulmonary  edema,  infarction,  and  atelecta- 
sis.  Atelectatic  crepitations  over  the  bases  and  borders  of  the  lungs 
are  common  in  persons  who  breathe  superficially,  either  from  habit 
or  from  weakness,  as,  for  example,  in  those  of  advanced  age,  whose 
breathing  is  habitually  shallow,  and  in  bed-ridden  patients,  whose 
alveoli  are  more  or  less  deflated  and  unduly  moist  through  disuse 
and  posture.  In  such  instances  a  brief  shower  of  fine  crepitations 
will  usually  be  heard  when  the  subject  takes  a  few  deep  inspirations 
of  sufficient  force  to  separate  the  walls  of  the  collapsed  vesicles  and 
infundibula;  ordinarily,  these  atelectatic  rales  disappear  after  the 
first  few  deep  breaths,  but  exceptionally  they  persist. 

Subcrepitant  Rales. — These  are  moist  bronchiolar  sounds,  audible 
during  both  inspiration  and  expiration,  and  due  to  the  force  expended 
by  the  air-columns  and  by  the  pulmonary  excursions  upon  the  con- 
tents of  the  ultimate  bronchial  tubes.  Owing  to  the  influence  of  these 
combined  forces,  deposits  of  viscid  secretion  are  snapped  apart  and 
torn  from  the  bronchiolar  mucosa,  minute  bubbles  of  thin  liquid 
are  exploded,  and  the  sticky  walls  of  some  of  the  finest  tubes  are 
alternately  agglutinated  and  separated.  The  moist  subcrepitations 
produced  in  this  manner  are  clicking  or  bubbling  or  crackling  sounds, 
which,  though  fine,  are  obviously  coarser  than  the  delicate  crepita- 
tions of  vesicular  origin.  They  are  not  unlike  the  succulent  sounds 
caused  by  agitating  a  mouthful  of  saliva  with  the  tongue,  when  the 
teeth  are  kept  in  contact  and  the  lips  apart. 

Subcrepitant  rales  indicate  the  presence  of  pathologic  secretion 
(serous,  serofibrinous,  purulent,  or  hemorrhagic)  within  the  bron- 
chioles, and  they  are,  therefore,  to  be  sought  for  in  catarrhal  pneu- 
monia, in  which  they  are  referable  to  an  exudative  bronchiolitis; 
in  the  third  stage  of  croupous  pneumonia,  when  the  bronchioles 
contain  a  liquefied  alveolar  exudate,  and  hence  afford  the  so-called 
rdle  rediix;  and  in  pulmonary  edema,  hemorrhage,  and  abscess,  in 
consequence  of  which  the  fine  tubes  are  flooded  with  serum,  blood, 
and  pus,  respectively.  In  incipient  phthisis  a  sharp,  high-pitched, 
clicking  sound,  known  as  the  mucous  click,  is  frequently  audible 


EXAMINATION   OF   THE   BRONCHOPULMONARY   SYSTEM       165 

during  deep  inspiration,  this  rale  being  essentially  a  subcrepitation 
indicative  of  a  tuberculous  catarrhal  bronchiolitis.  Atelectatic  sub- 
crepitations,  due  to  the  inspiratcry  separation  of  partly  collapsed  and 
agglutinated  bronchiolar  walls,  may  occur  under  the  conditions  respon- 
sible for  vesicular  crepitations  of  this  nature  (q.  v.  s.) . 

Mucous  Rales. — The  respiratory  passage  of  air  through  accumu- 
lations of  serum,  pus,  or  blood  in  the  larger  air-passages  produces 
various  sized  bubbling  and  explosive  sounds,  designated  as  mucous 
rales.  Such  rales  ordinarily  arise  within  the  bronchi,  less  commonly 
within  the  trachea  and  the  larynx,  and,  like  their  bronchiolar  counter- 
part, the  subcrepitant  rale,  are  audible  during  inspiration,  expiration, 
or  both ;  their  size,  intensity,  and  pitch  vary  according  to  the  diameter 
of  the  tube  in  which  they  originate.  With  air-columns  of  equal 
strength  and  with  a  secretion  of  the  same  density,  the  mucous  rales 
of  the  primary  bronchi  and  the  upper  respiratory  passages  are  coarser, 
louder,  less  numerous,  and  lower  pitched  than  those  of  the  medium- 
sized  bronchial  twigs,  between  the  primary  tubes  and  the  bronchioles. 
Clinically,  these  rales  are  usually  defined  as  large,  medium-sized, 
and  small,  according  to  the  impression  which  their  sound  conveys 
to  the  mind  of  the  auscultator.  Large-sized  mucous  rales  are  well 
illustrated  by  the  coarse,  intratracheal  blubbering  sounds  of  the 
"death-rattle";  smaller  types  of  these  rales,  by  the  more  delicate 
bubblings  heard  in  bronchitis. 

Coarse  gurgling  rales  are  produced  by  the  passage  of  air  through 
the  fluid  within  a  pulmonary  or  bronchiectatic  cavity,  whose  bronchial 
outlet  lies  below  the  upper  level  of  the  liquid  secretion  that  partly  fills 
the  excavation,  the  ebb  and  flow  of  air  through  the  fluid  exciting  a  series 
of  gurgling,  bubbling  noises  which  frequently  have  a  reverberating, 
metallic  quality  (Fig.  89).  Similar  rales  may  be  elicited  over  a  large 
bronchus  flooded  with  a  profuse  watery  secretion  (Fig.  88).  The 
size  and  the  pitch  of  gurgling  rales,  whether  pulmonary  or  bronchial, 
are  largely  determined  by  the  size  of  the  cavity  in  which  they  originate, 
the  coarseness  of  the  sound  increasing  and  its  pitch  lowering,  the 
larger  the  size  of  the  resonating  chamber.  Gurgling  rales  are 
most  clearly  heard  during  deep,  forcible  inspiration,  and  after  the 
act  of  coughing,  in  advanced  phthisis,  in  bronchiectasis,  and,  rarely, 
in  the  exudative  stage  of  bronchitis. 

The  pulmonary  fistula  sound  or  the  water-whistle  noise,  as  it  is  also 
called,  is  demonstrable  in  some  cases  of  valvular  pneumothorax 
(both  hydropneumothorax  and  pyopneumothorax)  in  which  the 
opening  of  the  pulmonary  fistula  lies  below  the  upper  level  of  the 
fluid  within  the  pleural  cavity.  This  being  the  case,  the  respiratory 


i66 


PHYSICAL    DIAGNOSIS 


movements  of  air  through  the  liquid  may  set  up  a  series  of  bubbling, 
gurgling  rales,  not  infrequently  endowed  with  a  metallic,  ringing 
quality. 

Cardiopneumatic  rdles,  or  moist  sounds  synchronous  with  the 
cardiac  action  and  usually  of  subcrepitant  or  of  crepitant  character, 
are  occasionally  audible  over  infiltrations  of  the  lung  immediately 
adjacent  to  the  heart.  Under  this  circumstance  rales  in  the  bron- 
chiolar  and  alveolar  secretion  may  be  generated,  partly  by  the  direct 
impact  of  the  heart  and  partly  by  the  sudden  variations  of  intra- 
thoracic  pressure  attending  systole  and  diastole. 

Pleural  Friction. — In  health  respiratory  excursions  of  the  moist, 
smooth  costal  and  pulmonary  pleurae  are  noiseless,  but  when  the 


Cavernous 
•gurgling 


Metallic  tinkle 
Succussion  sound 


Fig.  89. — Mechanism  of  cavernous  rales  and  splashing  sounds. 

pleural  surfaces  are  abnormally  dry  and  rough,  as  in  fibrinous  pleurisy 
and  in  tuberculosis,  their  movements  against  each  other  are  attended 
by  a  sound  known  as  pleural  friction,  whose  quality  and  intensity 
vary  greatly,  according  to  the  degree  and  extent  of  the  lesion.  (See 
Fig.  88).  The  friction-sound  is  in  some  instances  merely  a  delicate 
crepitation,  almost  indistinguishable  from  a  vesicular  rale;  in  others 
it  resembles  a  silken  rustle;  while  in  still  others  it  sounds  like  a  loud 
rasping  rub  or  like  the  crunching  of  dry  snow  underfoot.  It  is  more 
likely  to  be  an  interrupted  than  a  continuous  sound,  and  for  this 
reason  it  may  resemble,  at  least  superficially,  the  jerky  noise  of  cog- 
wheel breathing  (q.  v.  s.) .  Moreover,  it  is  a  superficial  and  often  quite 
circumscribed  sound,  intensified  by  the  pressure  of  the  stethoscope, 
practically  uninfluenced  by  the  act  of  coughing,  and  sometimes 


EXAMINATION   OF   THE    BRONCHOPULMONARY   SYSTEM 


i67 


accompanied  by  a  distinct  tactile  fremitus.  Friction  is  audible 
during  both  inspiration  and  expiration,  but  ordinarily  it  is  most 
distinct  toward  the  close  of  a  deep  inspiration.  Although  limited 
to  no  single  area  of  the  thorax,  pleural  friction  is  generally  most 
distinct  in  the  lower  axillary  region  on  the  affected  side,  and  just 
below  the  scapular  angle  (Fig.  90).  Should  a  patch  of  friction  dis- 
appear after  having  once  been  detected,  it  is  frequently  possible  to 
demonstrate  it  again  by  Abrams'  method  of  auscultating  over  the 
site  of  the  lesion  while  the  subject  sweeps  the  arm  of  the  affected  side 


Fig.  90. — Common  auscultatory  site  of  pleural  friction. 

upward  over  the  head,  thus  moving  the  two  pleural  surfaces  in  a 
direction  just  opposite  to  that  of  ordinary  respiration. 

Pleural  friction  is  heard  over  the  site  of  an  acutely  inflamed  dry 
pleura,  but  it  is  obscured  when  sufficient  exudate  accumulates  to 
lubricate  and  separate  the  inflamed  membranes;  with  the  resorption 
of  the  exudate,  however,  the  sound  reappears,  as  the  frictio  redux, 
which,  as  a  rule,  is  louder  than  the  primary  rub.  In  chronic  dry 
pleurisy  the  persistence  of  the  friction-sound  is  determined  by  the 
chronicity  and  the  progress  of  the  lesion.  Other  factors  that 
tend  to  destroy  the  normal  moist  and  smooth  state  of  the  pleurae, 


1 68  PHYSICAL   DIAGNOSIS 

and  hence  provoke  the  friction-rub,  are  tuberculosis,  neoplasms, 
and  profuse  diarrhea,  such  as  that  of  Asiatic  cholera,  which  inspis- 
sates the  pleural  cavities.  It  is  possible  that  certain  creaking 
sounds,  virtually  identical  with  those  of  genuine  pleural  friction, 
may  arise  from  inflammatory  changes  in  the  intercostal  muscles 
whereby  intermuscular  friction  is  excited  (Coplin).  The  pres- 
ence of  miliary  tubercles  beneath  the  pleura  may  be  sufficient 
to  produce  a  soft,  delicate  crepitation,  to  which  Reisman  has 
given  the  name  subpleural  crepitation.  Inflammation  of  the 
two  reflected  surfaces  of  the  complementary  pleura,  as  well  as 
subphrenic  peritonitis  and  perihepatitis,  account  for  friction- 
rubs,  not  infrequently  associated  with  tactile  fremitus,  over 
the  lower  right  thorax  below  the  sixth  rib  anteriorly,  the  eighth  rib 
laterally,  and  the  tenth  rib  posteriorly.  (See  Auscultation  of  the 
Abdomen.)  A  dry,  rubbing  sound  over  the  scapula,  known  as 
shoulder-blade  friction  (Duchenne),  may  be  due  to  the  friction  of 
this  bone  against  the  ribs,  normal  or  necrosed;  while  a  similar  sound 
in  the  same  situation  is  sometimes  indicative  of  what  Gee  describes 
as  shoulder -joint  friction,  this  sound  being  influenced  by  manipula- 
tion of  the  subject's  arm  and  becoming  louder  as  the  ear  approaches 
the  articulation. 

Perez's  sign,  friction  sounds  or  crackles  most  intense  over  the 
midsternum  on  movement  of  the  subject's  arms  at  the  shoulder- 
joint,  may  be  either  a  dry  pericardial  or  pleural  rub  generated  by 
mechanical  traction,  or  it  may  represent  merely  the  transmission 
of  an  articular  motor  crackle.  Ewart  emphasizes  the  importance 
of  clearly  differentiating  the  origin  of  this  sound  by  careful  aus- 
cultation with  a  view  of  localizing  it  to  the  shoulder-joint  or  to  an 
intrathoracic  area,  and  by  noting  the  effects  of  articular  move- 
ments and  of  respiration  upon  the  vibrations. 

Pleuropericardial  friction  is  audible,  most  commonly  toward  the 
left  border  of  the  precordia,  from  the  effect  of  the  cardiac  impact 
against  the  adjacent  pleural  surfaces,  roughened  by  fibrinous  inflam- 
matory deposits.  Obviously,  such  sounds  are  synchronous  with  the 
movements  of  the  heart,  and  it  is  also  true  that  they  bear  a  distinct 
relation  to  the  respiratory  phases.  If  the  roughening  implicates 
the  pericardial  and  the  pulmonary  reflections  of  the  pleura,  the 
friction  diminishes  or  quite  disappears  at  the  end  of  deep  expiration, 
for  during  the  recession  of  the  deflated  pulmonary  border  over  the 
heart  the  two  inflamed  surfaces  are  not  in  contact  (Fig.  91).  If, 
on  the  other  hand,  the  lesion  be  situated  upon  the  pericardial  and 


EXAMINATION    OF    THE    BRONCHOPULMONARY    SYSTEM       169 

the  costal  pleurae,  the  friction  becomes  enfeebled  or  lost  at  the  end 
of  forced  inspiration,  or  when  the  inflated  pulmonary  border  inter- 


Expiration. 
nouyfietied  bleurae  afiart~.  RricarduU 


Inspiration. 
Jfouyhened jaleurOf  in  cordacf. 


Fig.  9  1.  —  Mechanism  of  pleuropericardial  friction,  audible  during  inspiration,  but 
inaudible  during  expiration. 

venes  to  separate  the  two  roughened  membranes  (Fig.  92).    The 
differentiation  of  this  pleuropericardial  or  extrapericardial  friction 


Expiration. 


Inspiration. 


Fig.  92. — Mechanism  of  pleuropericardial  friction,  audible  during  expiration,  but 
inaudible  during  inspiration. 

and  that  of  pericardial  origin  is  described  elsewhere.     (See  Peri- 
cardial  Friction,  p.  389.) 


SPLASHING    SOUNDS 


Succussion  Sounds. — The  presence  of  air  and  fluid  within  a  body 
cavity  is  determined  by  succussion,  or  the  act  of  suddenly  shaking  the 
subject  so  as  thus  to  create  audible  waves,  recognized  as  succussion 
sounds  (Fig.  89).  These  sounds  are  best  appreciated  by  stethoscopic 
auscultation,  but  sometimes  they  are  audible  at  some  distance  from  the 


1 70  PHYSICAL   DIAGNOSIS 

subject,  who,  indeed,  may  be  conscious  of  the  splashing  sensation. 
Succussion  sounds  are  highly  suggestive  of  air  and  fluid  within 
the  pleural  cavity,  their  association  with  pneumothorax  having 
been  first  described  by  Laennec — though  Hippocrates  was  unques- 
tionably the  discoverer  of  intrathoracic  splashing  (Hippocratic 
succussion  sound),  he  misinterpreted  it  as  a  sign  of  empyema. 
The  sounds,  which  generally  have  a  hollow,  metallic  tone,  are  most 
commonly  detected  in  hydropneumothorax,  less  frequently  in  pyo- 
pneumothorax,  and  exceptionally  they  are  audible  over  a  large 
pulmonary  cavity  containing  fluid.  Splashing  sounds  arising  within 
the  stomach  and  the  large  intestine  are  distinguished  from  those 
of  intrapleural  origin  by  an  analysis  of  the  associated  physical 
signs  and  the  localization  of  the  sounds.  Exceptionally  a  succus- 
sion wave  can  be  recognized  by  palpation. 

Metallic  Tinkling. — This  sound,  also  termed  the  "falling-drop 
sound"  (gutta  cadens),  resembles  the  hollow,  metallic  tinkling  of 
drops  of  water  falling  from  a  height  upon  the  surface  of  the  fluid 
within  a  partly  rilled  cistern  (Fig.  89).  A  metallic  tinkle  is  con- 
stantly audible  in  hydropneumothorax  and  pyopneumothorax,  in 
which  conditions  it  is  provoked  by  deep  breathing,  loud  speaking, 
coughing,  and  changes  in  the  subject's  posture.  Several  credible  fac- 
tors have  been  advanced  to  explain  this  physical  sign :  the  dropping 
of  fluid  from  the  edges  of  the  moist,  retracted  lung  above  upon  the 
surface  of  the  pleural  effusion  below;  the  explosion  of  moist 
rales  at  the  outlet  of  a  pulmonary  fistula  situated  above  the 
level  of  the  fluid;  and  the  bursting  of  small  bubbles  upon  the 
surface  of  the  effusion.  Metallic  tinkling  must  be  distinguished 
from  the  metallic  consonating  rales  to  be  heard  over  a  pulmonary 
cavity,  from  the  reverberations  of  transmitted  bronchial  rales,  and 
from  the  succulent  sounds  arising  in  a  pneumothoracic  fistula. 


SECTION   IV 

DISEASES   OF   THE    BRONCHOPULMONARY   SYS- 
TEM AND  MEDIASTINUM 


ACUTE     CATARRHAL     BRONCHITIS     (Acate     Tracheobronchitis; 
Acute    Bronchial     Catarrh) 

Clinical  Pathology. — The  term  acute  bronchitis,  or  tracheo- 
bronchitis,  is  applicable  to  a  catarrhal  inflammation,  either  general 
or  circumscribed,  affecting  the  mucosa  of  the  trachea  and  bronchial 
tubes,  but  not  extending  to  the  bronchioles.  Should  the  latter  also 
be  implicated  (bronchiolitis),  extension  to  the  air-vesicles  (vesiculitis) 
is  certain  to  occur,  which  two  changes  together  constitute  broncho- 
pneumonia.  The  designation  of  this  condition  as  a  "capillary  bron- 
chitis" is  unwarranted  on  pathologic  grounds. 

The  changes  in  the  tracheobronchial  mucosa  consist  of  a  primary 
hyperemia  and  moderate  tumefaction,  with  degeneration  and  des- 
quamation  of  the  epithelium,  followed  by  swelling  and  hypersecretion 
of  the  mucous  glands.  As  a  rule,  the  exudate  that  bathes  the  inflamed 
membranes  is  mucous  or  serous,  though  it  may  have  a  more  or  less 
purulent  character.  According  to  the  intensity  of  the  process,  a 
variable  number  of  round-cells  infiltrate  the  mucosa  and  submucosa, 
but,  save  in  extremely  severe  cases,  this  process  does  not  permeate 
far  into  the  bronchial  walls.  Ordinarily,  the  inflammation  subsides 
without  complications  or  sequelae,  and  the  mucosal  swelling  promptly 
disappears,  the  epithelium  regenerates,  the  infiltrations  are  absorbed, 
and  the  secretions  are  removed  by  expectoration,  leaving  the  mucous 
membrane  of  the  affected  parts  intact  and  normal.  Less  commonly, 
the  disease  becomes  chronic,  and  leads  to  extensive  denudation  and 
ulceration  of  the  mucosa,  and  perhaps  to  permanent  structural 
changes  in  the  walls  of  the  bronchi. 

Acute  bronchitis  is  usually  secondary  to  a  catarrhal  inflammation 
of  the  upper  air-passages,  which,  by  extension  downward,  invades  the 
trachea  and  the  bronchial  tree;  or,  it  may  be  symptomatic  of  some 
infectious  disease — measles,  influenza,  enteric  fever,  malarial  fever, 

171 


172  PHYSICAL   DIAGNOSIS 

pertussus,  phthisis,  or  pneumonia.  The  direct  inhalation  of  irri- 
tant vapors,  the  insufflation  of  contaminated  material  from  the 
upper  respiratory  tract,  and  the  lodgment  of  a  foreign  body  in  an 
air-passage  are  additional  factors  of  bronchial  inflammation. 
A  fulminant  type  of  bronchitis,  with  a  primary  outpouring  of  thin 
frothy  mucus  followed  by  a  secretion  of  thick  mucopurulent  matter, 
attends  the  asphyxial  stage  of  chlorin  gassing,  numerous  examples  of 
which  have  been  reported  among  the  troops  of  the  British  Expedi- 
tionary Force  in  France  during  the  present  Continental  war;  and  in 
fatal  cases  intense  pulmonary  congestion  and  edema,  with  multiple 
patches  of  acute  marginal  emphysema,  are  the  usual  sequelae  (Her- 
ringham).  Fungus  tracheobronchitis,  due  to  various  identified  and 
non-determined  fungi,  is  frequently  met  with  in  the  tropics.  The 
chronic  bronchitides  attending  gout,  cardiorenal  disease,  asthma, 
and  emphysema  have  from  time  to  time  ingrafted  upon  them  acute 
exacerbations,  which  to  all  intents  and  purposes  may  be  regarded  as 
attacks  of  acute  bronchitis. 

Physical  Signs. — Inspection. — In  simple  acute  bronchitis  the 
information  gained  by  inspection  is  more  likely  to  be  negative  than 
positive.  The  thoracic  expansion  is  symmetric,  no  anomalies  of  the 
respiratory  movements  are  found,  and  the  normal  rhythm  and  rate 
of  breathing  remain  undisturbed,  except  for  a  moderate  polypnea, 
accompanied  by  a  proportionate  increase  in  the  rapidity  of  the  pulse, 
when  the  attack  is  attended  by  considerable  fever.  Actual  dyspnea 
is  seldom  seen,  save  in  the  event  of  bronchiolitis  and  of  severe  sub- 
sternal  pain. 

Palpation. — Vocal  fremitus,  as  a  rule,  is  normal,  although  it  may 
be  temporarily  diminished  or  quite  cut  off  over  a  circumscribed  area 
of  the  lung,  should  the  bronchus  leading  to  such  an  area  be  plugged 
by  a  bit  of  secretion;  when  the  obstruction  is  expelled  by  coughing, 
however,  the  voice  vibrations  immediately  reappear.  Rhonchal 
fremitus  is  palpable,  especially  during  active  inspiration,  when  the 
tubes  contain  considerable  secretion. 

Percussion. — Normal  pulmonary  resonance  is  unimpaired,  so  long 
as  the  inflammation  is  restricted  to  the  larger  bronchi,  but  should 
it  extend  to  the  bronchioles  and  the  neighboring  alveoli,  as  it  is  prone 
to  do  in  the  extremes  of  life,  patches  of  dulness,  usually  first  detected 
at  the  bases,  appear.  As  the  result  of  alveolar  overinflation,  areas 
of  moderate  hyperresonance  are  sometimes  demonstrable,  particularly 
over  the  upper  regions  of  the  chest. 

A  uscultation. — The  respiratory  murmur  may  be  normal,  enfeebled, 
or  harsh:  normal,  so  long  as  the  air-currents  traverse  the  bronchi 
without  hindrance;  enfeebled,  if  not,  indeed,  absent,  if  the  lumen  of 


DISEASES    OP    THE    BRONCHOPULMONARY    SYSTEM         173 

a  tube  be  blocked  by  secretion ;  and  harsh,  often  with  prolongation 
of  expiration,  if  the  bronchial  caliber  be  decidedly  narrowed  by  a 
swollen,  secretion-laden  mucosa.  Vocal  resonance  behaves  like 
vocal  fremitus.  Bronchial  rales  are  audible  during  both  inspiration 
and  expiration,  and  can  usually  be  made  to  appear  and  disappear 
by  instructing  the  patient  to  cough  deeply  and  to  breathe  forcibly. 
In  the  early,  dry  stage  of  bronchitis  low-pitched,  sonorous,  and  piping 
sibilant  rales  predominate,  but  later,  as  the  liquid  secretion  accumu- 
lates, numerous  mucous  bubblings  are  also  audible,  the  two  types 
of  adventitious  sounds  persisting  so  long  as  the  air-tubes  are  narrowed 
by  inflammation  and  filled  with  secretion. 

Diagnosis.— Acute  bronchitis  presents  a  group  of  distinctive 
physical  signs — harsh  breathing  and  widely  disseminated  dry  and 
moist  bronchial  rales,  with  no  impairment  of  the  normal  tactile 
fremitus  and  pulmonary  resonance.  Add  to  these  findings  a  history 
of  having  "taken  cold,"  and  of  coryza,  hoarseness,  substernal  pain, 
and  cough,  with  little  or  no  fever,  and  the  diagnosis  is  complete. 

The  possibility  of  mistaking  pulmonary  tuberculosis  for  simple 
bronchitis  should  always  be  thought  of,  since  incipient  phthisis  may 
show  little  else  than  bronchitic  signs,  which,  if  persistent,  are  highly 
suggestive.  In  doubtful  cases  apical  localization  of  such  signs  is 
to  be  sought  for,  the  sputum  stained  for  tubercle  bacilli,  and  a  minute 
study  made  of  the  expansion,  fremitus,  resonance,  and  breath-sounds. 

Bronchopneumonia,  in  affording  little  else  than  a  chestful  of  widely 
disseminated  bronchial  rales,  may  closely  resemble  a  simple  acute 
catarrh  affecting  especially  the  smaller  bronchi.  But  in  broncho- 
pneumonia,  despite  the  absence  of  tubular  breathing  and  dulness,  it 
is  often  possible  to  distinguish,  amid  the  medley  of  rhonchi,  the  fine 
subcrepitant  and  crepitant  rales  betraying  bronchiolar  and  alveolar 
implication,  together  with  undue  prolongation  of  expiration  and 
unnatural  hyperresonance.  When  these  distinctive  evidences  of 
multiple  small  lobular  consolidation  are  not  apparent,  the  diagnosis 
must  rest  upon  such  details  as  urgent  dyspnea,  cyanosis,  and 
hyperpyrexia,  which  are  conspicuous  signs  of  a  bronchopneumonic 
process. 

Occasionally,  croupous  pneumonia  is  counterfeited  by  a  bronchitis 
that  begins  abruptly  with  a  chill,  considerable  fever,  and  blood- 
stained expectoration,  and  in  such  cases  the  wide-spread  distribution 
and  bronchitic  character  of  the  physical  signs  and  the  absence  of 
evidences  of  lobar  consolidation  indicate  bronchial  inflammation. 

Exceptionally,  the  early  symptoms  of  some  infectious  disease  are 
temporarily  masked  by  a  coexisting  bronchitis,  as  in  certain  cases 
of  enteric  fever,  malarial  fever,  pertussis,  and  measles.  In  such 


174  PHYSICAL   DIAGNOSIS 

instances  the  experienced  examiner,  without  waiting  for  a  complete 
clinical  picture  to  develop,  is  frequently  able  to  identify  the  asso- 
ciated infection  by  finding  some  one  distinctive  sign,  such  as  a  posi- 
tive blood-culture  in  typhoid,  the  presence  of  parasites  in  malaria, 
a  mononucleosis  in  pertussis,  and  Koplik's  spots  in  measles. 

CHRONIC  CATARRHAL  BRONCHITIS  (Chronic  Bronchial  Catarrh; 
Winter  Cough) 

Clinical  Pathology. — In  chronic  bronchitis  the  bronchial  mucosa 
shows  a  variable  degree  of  persistent  hyperemia,  together  with 
epithelial  denudation,  granular  changes,  and  foci  of  ulceration. 
There  is  also  .round-cell  infiltration,  either  implicating  merely  the 
mucous  and  submucous  tissues,  or  extending  through  the  entire 
bronchial  wall,  and  perhaps  leading  to  peribronchitis  and  peri- 
bronchial  adenitis.  In  the  course  of  time  serious  defects  in  the 
tubes  tend  to  supervene — destruction  of  the  mucous  glands,  local 
patches  of  atrophy  and  hyperplasia,  areas  of  necrosis  and  ulceration, 
and  bronchiectatic  dilatations  of  various  shape  and  size.  Emphy- 
sema is  a  practically  constant,  and  cirrhosis  a  common,  associated 
pulmonary  change.  The  retained  bronchial  secretion  may  consist 
of  thin,  serous  fluid,  glairy  mucus,  mucopus,  or  fetid  purulent  matter. 

Chronic  bronchitis  is  sometimes  traceable  to  a  single  attack  of  acute 
bronchial  inflammation  incident  to  some  one  of  the  acute  infections, 
but  more  often  it  is  but  the  relic  of  repeated  bronchial  catarrhs. 
The  familiar  "winter  cough"  of  old  persons  means  simply  the  annual 
lighting  up  of  an  old  bronchitis  that  has  smouldered,  quiescent, 
during  the  warm  months.  In  many  instances,  if  not  in  most,  the 
cause  is  primarily  cardiac,  renal,  pulmonary,  arterial,  or  gouty. 
Aneurism  of  the  aortic  arch  is  also  to  be  recalled  as  a  possible  cause 
of  intractable  bronchial  inflammation. 

Physical  Signs. — The  physical  signs  of  chronic  bronchitis  are 
in  no  sense  distinctive,  for  they  depend  not  only  upon  the  changes  in 
the  bronchial  mucosa  and  wall,  but  also  upon  the  character  of  the 
associated  lesions,  pulmonary,  cardiovascular,  or  renal,  as  the  case 
may  be.  In  general,  the  findings  resemble  those  of  the  acute  type, 
but  they  are  not  so  .constant,  clear  cut,  or  well  defined,  and  in  most 
cases  the  coexisting  emphysema  and  asthhia  conspicuously  modify 
the  physical  signs. 

Inspection  and  palpation  show,  sooner  or  later,  that  the  chest  is 
overdistended,  that  the  respiratory  movements  are  restricted  and 
labored,  and  that  vocal  fremitus  is  feebler  than  normal.  Percussion, 
though  frequently  showing  nothing  abnormal,  may  yield  a  general 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        175 

hyperresonance  referable  to  habitual  overdistention  of  the  vesicu- 
lar structure.  Auscultation  reveals  undue  expiratory  prolongation, 
a  confusing  commingling  of  normal,  feeble,  and  harsh  breathing,  and 
various  sized  dry  and  moist  bronchial  rales,  indicative  of  different 
degrees  of  dry  and  exudative  inflammation  within,  and  spasmodic 
stenosis  of,  various  parts  of  the  bronchial  tree.  Should  there  be 
patches  of  collapsed  lung  at  the  bases,  as  is  commonly  the  case,  basal 
crepitation  can  be  distinguished. 

Diagnosis. — Having  diagnosed  chronic  bronchitis  by  the  fore- 
going signs,  it  is  important  to  determine  whether  the  process  be 
primary  or  secondary  to  some  organic  disease,  and  also  whether 
it  be  associated  with  emphysema,  asthma,  bronchial  dilatation,  or 
other  complications. 

Aside  from  simple  chronic  bronchitis,  the  following  three  special 
varieties  are  of  clinical  interest:  Dry  catarrh,  or  Laennec's  catarrhe 
sec,  distinguished  by  scanty,  tenacious  sputum,  by  severe  fits  of  cough- 
ing, and  by  its  common  association  with  emphysema;  bronchorrhea, 
in  which  there  are  severe  paroxysms  of  cough,  productive  of  aston- 
ishingly large  quantities  of  bronchial  secretion,  consisting  either  of 
mucopurulent  matter,  or,  less  commonly,  of  thin,  frothy,  odorless 
mucus — the  so-called  mucous  catarrh,  or  Laennec's  catarrhe  pit- 
uiteux;  fetid  or  putrid  bronchitis,  characterized  by  disgustingly  fetid 
expectoration,  composed  largely  of  pus,  detritus,  fatty  acids,  bacteria 
and  various  fungi,  and  frequently  containing  minute  yellowish- 
brown  masses — Dittrich's  or  Traube's  plugs.  Rigors,  fever,  anemia, 
emaciation,  and  similar  evidences  of  septic  poisoning  may  develop 
in  fetid  bronchitis,  and  in  some  instances  extensive  damage  to  the 
bronchial  walls,  pulmonary  infection,  and  embolic  lesions  of  distant 
organs  occur.  True  fetid  bronchitis  should  not  be  diagnosed  by 
the  odor  of  the  sputum  alone,  for  the  stench  may  be  quite  as  bad 
in  bronchiectasis,  pulmonary  abscess,  gangrene,  tuberculosis,  and 
perforative  empyema. 

FIBRINOUS  BRONCHITIS  (Plastic  Bronchitis) 
Clinical  Pathology. — This  rare  type  of  bronchial  inflammation 
is  distinguished  by  the  formation,  within  the  finer  bronchial  tubes, 
of  fibrinous  casts  which  become  detached  and  are  expectorated  in 
the  form  of  small  gray  or  yellowish  plugs  or  molds.  These  plugs 
can  be  teased  out  into  dendritic  bronchial  molds,  of  either  tubular 
or  solid  structure,  and  composed  usually  of  mucin,  but  rarely  of 
fibrin.  With  these  masses  erythrocytes,  leukocytes,  epithelial  cells, 
and  Charcot-Leyden  crystals  are  incorporated,  and  to  their  dendritic 
extremities  Curschmann's  spirals  are  commonly  attached.  The 


176  PHYSICAL   DIAGNOSIS 

bronchial  surface  where  the  membrane  forms  is  not  conspicuously 
affected:  pallor  or  hyperemia  of  the  mucosa,  its  epithelium  either 
remaining  intact  or  being  denuded,  and  moderate  tumefaction  and 
infiltration  of  the  submucosa  being  the  ordinary  changes. 

Physical  Signs. — Inspection. — Paroxysms  of  urgent  dyspnea  and 
coughing,  perhaps  with  cyanosis  and  hemoptysis,  are  the  noteworthy 
signs  during  the  loosening  and  subsequent  expectoration  of  the  casts. 
Should  one  of  the  larger  bronchial  passages  be  obstructed,  there  may 
be  inspiratory  retraction  of  the  lower  intercostal  spaces  on  the  affected 
side. 

Palpation. — Ordinarily,  the  voice  vibrations  are  unaltered,  save 
in  the  event  of  bronchial  occlusion  and  as  the  result  of  a  complicating 
pneumonic  consolidation,  the  fremitus  being  enfeebled  or  abolished 
in  the  former  and  exaggerated  in  the  latter.  When  bronchial  rales 
are  plentiful,  their  vibrations  are  appreciable  to  the  palpating  hand. 

Percussion. — The  percussion  sound  over  the  lungs  may  be  resonant, 
hyperresonant,  or  frankly  dull,  according  to  the  condition  of  the  vesic- 
ular structure — whether  normal,  emphysematous,  or  consolidated. 
Ordinarily,  however,  there  is  more  or  less  general  exaggeration  of 
the  normal  pulmonary  resonance. 

Auscultation. — In  uncomplicated  cases  the  respiratory  murmur 
is  either  suppressed  or  harsh,  with  a  prolonged  expiratory  phase. 
Unnatural  sharpening  and  intensity  of  the  breathing  should  prompt 
a  careful  search  for  a  patch  of  lobular  or  of  lobar  consolidation. 
Many  moist  and  dry  rales  are  audible,  notably  the  peculiar  dry 
"bruit  de  drapeau,"  due  to  the  oscillations  of  bits  of  partly  detached 
bronchial  membrane.  (See  p.  163.) 

Diagnosis. — The  physical  signs  of  bronchitis  and  the  expectora- 
tion of  branching  molds  of  the  smaller  bronchi,  together  point  to 
fibrinous  bronchitis,  but,  aside  from  these  distinctive  findings,  it 
is  well  also  to  investigate  the  patient's  previous  history.  Two 
types  of  the  affection  are  recognized:  a  chronic  recurrent  form,  appar- 
ently idiopathic,  and  characterized  by  paroxysms  tending  to  recur 
periodically  year  after  year,  at  approximately  regular  intervals; 
and  an  acute  form,  of  rarer  occurrence  and  graver  outlook,  which 
commonly  complicates  one  of  the  febrile  infections,  and  is  distin- 
guished by  dyspneic  paroxysms  of  alarming  severity,  ushered  in  by 
a  sharp  attack  of  bronchitis,  and  attended  by  fever  and  rigors. 

True  fibrinous  bronchitis  of  the  foregoing  types  is  to  be  distin- 
guished from  certain  conditions  sometimes  attended  by  the  accumu- 
lation of  fibrin,  membrane,  or  blood  within  the  bronchial  tubes. 
Fibrinous  molds  of  the  bronchi,  for  example,  are  occasionally  expec- 
torated in  pneumonia,  diphtheria,  phthisis,  chronic  cardiac  disease, 


DISEASES    OF    THE   BRONCHOPULMONARY    SYSTEM        177 

and  after  paracentesis  of  a  pleural  exudate.  The  sputum  may  con- 
tain blood  coagula  in  bronchopulmonary  hemorrhage,  and  fungus 
casts  in  pulmonary  aspergillosis. 

BRONCHIAL  ASTHMA   (Spasmodic,  Essential,  Idiopathic,   or  Catar- 

rhal  Asthma) 

Clinical  Pathology. — The  respiratory  neurosis,  known  as  bron- 
chial asthma,  is  distinguished  clinically  by  recurrent,  often  periodic, 
paroxysms  of  dyspnea,  cough,  and  viscid  expectoration,  accompanied 
by  inspiratory  thoracic  rigidity  and  overdistention,  and  by  depression 
and  restricted  mobility  of  the  diaphragm.  Spasm  of  the  bronchial 
muscles,  commonly  attended  by  hyperemia  and  swelling  of  the  mucosa 
of  the  smaller  tubes  and  by  a  peculiar  viscid  bronchiolar  secretion, 
chiefly  explains  the  asthmatic  attack.  The  bronchial  spasm  of  itself 
is  sufficient  to  interfere  with  the  passage  of  air  through  the  finer  tubes, 
and  the  blocking  of  their  lumen  by  a  turgescent  mucosa  and  by 
clumps  of  sticky  mucus  still  further  increases  the  difficulty.  In 
addition,  as  Alexander  Morison  points  out,  there  is  also  a  relative, 
if  not  an  actual,  impediment  to  the  ingress  of  air,  and  an  actual 
impediment  to  its  egress,  owing  to  the  great  increase  in  the  relative 
volume  of  residual  intrapulmonary  air  existing  during  the  asthmatic 
seizure.  Repeated  attacks  of  asthma  lead  to  the  development  of 
chronic  bronchial  catarrh,  emphysema,  and  dilatation  of  the  right 
heart,  and  the  changes  incident  to  these  complications  and  sequelae 
are  the  important  pathologic  findings  of  this  neurosis. 

In  a  person  predisposed  to  asthma  the  paroxysms  may  be  pre- 
cipitated by  an  almost  endless  diversity  of  causes — by  emotional  dis- 
turbances, fatigue,  and  similar  factors  having  a  central  action; 
by  climatic  peculiarities,  irritating  dust,  unpleasant  odors,  and  the 
respiratory  strain  of  violent  coughing,  laughing,  or  sneezing,  which 
probably  produce  bronchial  stimulation;  by  reflex  waves  propagated 
from  distant  parts,  as  in  the  attacks  excited  by  nasal  lesions,  dys- 
pepsia, and  utero-ovarian  disorders.  Sometimes  asthma  supervenes 
after  bronchitis,  pertussis,  or  pneumonia,  and  sometimes  it  is  directly 
related  to  vagus  irritation  depending  upon  mediastinal  pressure. 

Physical  Signs. — Inspection. — During  the  attack  the  patient's 
chest  is  in  a  state  of  undue  inspiratory  distention,  the  respiratory 
movements  are  labored,  limited,  and  inefficient,  and  the  excursion 
of  the  diaphragm  is  greatly  restricted.  Beginning  as  a  mere  oppres- 
sion in  breathing,  the  dyspnea  becomes  more  and  more  urgent  until, 
as  the  acme  of  the  paroxysm  is  reached,  orthopnea  supervenes, 


1 78  PHYSICAL   DIAGNOSIS 

bringing  into  active  play  the  auxiliary  muscles  of  respiration,  and 
compelling  the  subject  to  rush  to  an  open  window  in  his  desperate 
fight  for  air.  At  this  stage  of  the  attack  frequently  there  are  cyan- 
osis, subnormal  temperature,  and  a  feeble  running  pulse;  inspiration 
amounts  to  little  more  than  a  series  of  short,  jerky  gasps,  while  expir- 
ation is  laboredly  prolonged  and  wheezy,  the  whole  picture  being  one 
of  acute  expiratory  dyspnea,  for  deflation  of  the  lungs  is  the  main 
difficulty.  As  the  acme  of  the  attack  passes,  often  with  a  violent 
fit  of  coughing,  the  breathing  becomes  easier,  the  cyanosis  disappears, 
and  the  patient,  exhausted,  may  fall  into  a  deep  sleep.  The  cough, 
until  this  time  tight  and  unproductive,  now  loosens  and  the  patient 
expectorates  copiously,  much  to  the  relief  of  the  respiratory  distress. 
Early  in  the  attack  the  sputum  is  scanty,  and  consists  largely  of  little 
pearly  beads  of  glairy  mucus  (Laennec's  "perles"),  which,  when 
unrolled,  are  found  to  be  bronchiolar  casts  having  a  peculiar  spiral 
structure.  These  so-called  Curschmann's  spirals  are  composed  of 
strands  of  mucin  twisted  into  a  tight  coil  in  whose  meshes  numerous 
leukocytes  (especially  eosinophiles) ,  bronchiolar  epithelium,  and  per- 
haps Charcot-Leyden  crystals  are  entangled.  Some  of  these  spiral 
bodies  are  provided  with  a  clear,  translucent  core,  probably  com- 
posed of  a  filament  of  transformed  mucin.  As  the  cough  loosens, 
with  the  decline  in  the  intensity  of  the  paroxysm,  the  now  abundant 
sputum  becomes  of  a  mucopurulent  character,  and  no  longer  con- 
tains the  Curschmann  spirals.  Blood-streaked  sputum  is  common 
in  severe  paroxysms  attended  by  active  bronchitis. 

Other  physical  signs  sometimes  observed  during  an  attack  of 
asthma  include  erythema,  urticaria,  and  angioneurotic  edema  of 
the  upper  extremities  (J.  S.  Billings,  Jr.).  Very  exceptionally, 
cervical  emphysema  is  produced  by  the  violent  strain  of  coughing. 

Palpation. — During  the  paroxysm  the  pulmonary  overdistention 
and  the  bronchial  obstruction  together  enfeeble,  if  not  abolish,  vocal 
fremitus;  during  the  interval,  provided  that  permanent  emphysema 
does  not  exist,  the  voice  vibrations  are  normally  transmitted.  Pro- 
nounced rhonchal  fremitus  is  a  familiar  tactile  sign.  The  pulse 
is  likely  to  be  feeble,  rapid,  and  intermittent  or,  indeed,  imperceptible 
during  inspiration,  and  the  cardiac  apex-beat  may  be  effectually 
obscured  by  the  overdilated  pulmonary  tissue. 

Percussion. — The  percussion  sound  is  abnormally  resonant  over 
both  lungs,  except,  in  some  instances,  at  the  bases,  where  impaired 
resonance  from  atelectasis  may  be  detected.  Should  decided  em- 
physematous  distention  of  the  lungs  exist,  the  normal  areas  of 
hepatic,  cardiac,  and  splenic  flatness  are  correspondingly  encroached 
upon. 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        179 

Auscultation. — The  respiratory  murmur  and  the  cardiac  sounds 
are  masked  by  a  pandemonium  of  rales,  loud  and  sonorous  tones 
commingled  with  shrill  and  cooing  sounds,  occurring  early  in  the 
attack,  while  small  and  coarse  mucous  bubbling  is  audible  during 
and  after  the  acme  of  dyspnea.  The  patient,  as  Salter  happily 
expresses  it,  wheezes  "  as  if  a  whole  orchestra  of  fiddles  were  tuning 
in  his  chest,"  and  oftentimes  the  rales  are  so  loud  that  they  are  dis- 
tinctly heard  some  distance  from  the  patient's  chest;  dry  rales  and 
mucous  sounds  tend  to  persist,  after  the  acute  seizure  is  past,  so  long 
as  secretion  remains  within  the  bronchial  passages.  The  alterations 
in  vocal  resonance  correspond  to  those  of  vocal  fremitus. 

Diagnosis. — An  asthmatic  paroxysm  is  clearly  recognized  by 
the  physical  signs,  of  which  urgent  expiratory  dyspnea,  hyperreson- 
ance,  loud  rhonchi,  and  viscid,  pearly  sputum  form  a  distinctive 
group.  These  signs,  plus  the  case-history,  serve  to  separate  asthma 
from  acute  bronchitis,  pleurisy,  phthisis,  and  pneumonia  attended 
by  excessive  dyspnea,  cyanosis,  and  restricted  movements  of  the  chest. 

Pertussis,  with  its  sudden  attacks  of  difficult  breathing,  is  not 
unlike  asthma,  but  in  whooping-cough  the  characteristic  "crow," 
the  laryngeal  cough,  and  the  inspiratory  type  of  dyspnea  are  dis- 
tinctive criteria. 

Certain  forms  of  toxic  dyspnea,  as  well  as  anemic  shortness  of  breath, 
are  readily  differentiated  from  bronchial  asthma,  when  the  physical 
signs  and  the  patient's  history  are  studied.  So-called  renal,  cardiac, 
and  anemic  "asthmas' '  are  misnamed — "dyspnea' '  is  the  proper  term 
for  such  disturbances,  which  are  in  no  way  related  to  true  bronchial 
asthma. 

BRONCHIECTASIS   (Bronchial  Dilatation) 

Clinical  Pathology. — Bronchiectasis  is  a  circumscribed  or  a 
general  dilatation  of  the  bronchial  tubes,  of  which  two  principal 
types  are  recognized:  the  cylindric,  or  fusiform,  which  affects  the 
entire  bronchial  circumference,  usually  of  the  larger  bronchi;  and 
the  saccular,  or  globular,  in  which  the  lesion  consists  of  a  pouch-like 
expansion  or  of  a  series  of  pockets,  commonly  implicating  the  smaller 
tubes  (Fig.  93).  The  term  bronchiolectasis  is  used  to  designate  that 
uncommon  condition  of  extensive  dilatation  of  the  bronchioles  met 
with  almost  exclusively  in  the  young  child.  Bronchiectasis  univer- 
salis,  also  a  rare  form  of  the  disease,  is  a  congenital  affection,  in  which 
one  entire  bronchial  tree  is  converted  into  a  series  of  irregular  sac- 
culations. 

Bronchiectasis  is  most  commonly  situated  at  the  pulmonary  bases, 
except  in  the  tuberculous  form,  which  ordinarily  is  apical.  Unilateral 


i8o 


PHYSICAL    DIAGNOSIS 


dilatation  is  a  shade  more  common  than  bilateral,  and  in  the  former, 
implication  of  the  right  and  the  left  bronchi  occurs  with  about  equal 
frequency.  In  bilateral  bronchiectasis  the  lesion  is  prone  to  be  much 
more  extensive  in  one  bronchial  tree  than  in  the  other. 

Acquired  bronchiectasis  is  due  primarily  to  weakening  and  lowered 
resiliency  of  the  bronchial  wall,  which  gives  way  under  the  stress 
of  increased  internal  pressure  or  from  external  traction,  and  thereby 


Bronchial  cavities 


Enlarged  peribronchiaJ 
lymph-nodes 


Bronchial  cavities 


Fig.  93. — Bronchiectasis  (Jefferson  Hospital  Laboratories). 

enlarges  the  bronchial  lumen  wherever  such  damage  exists.  Inflam- 
matory mural  changes,  the  strain  of  coughing,  the  pressure  of  a  large 
volume  of  intrabronchial  secretion,  and  the  traction  exerted  by  peri- 
bronchial  adhesions  are  the  exciting  factors  essential  to  the  formation 
of  the  ectases.  The  most  important  affections  in  which  they  develop 


DISEASES    OF    THE   BRONCHOPULMONARY    SYSTEM        l8l 

secondarily  include  chronic  bronchitis,  tuberculosis,  pleurisy,  croup- 
ous  and  catarrhal  pneumonia,  influenza,  pulmonary  cirrhosis,  ate- 
lectasis,  emphysema,  and  bronchial  obstruction  from  external  press- 
ure by  foreign  bodies. 

The  pathologic  changes  in  the  dilated  tubes  are  extremely  variable, 
according  to  the  character,  degree,  and  duration  of  the  disease.  In 
active,  acute  cases  the  mucosa  has  the  familiar  appearance  of  acute 
bronchial  inflammation.  In  bronchiectases  of  decided  chronicity, 
however,  the  damage  is  much  more  extensive  at  the  seat  of  ectasis, 
as  shown  by  wasting  of  the  muscular  and  elastic  coats,  by  fibrous 
thickening,  and  by  ulceration  of  the  mucosa.  Indeed,  in  some 
instances  little  or  no  trace  of  the  bronchial  structure  remains,  the 
lesion  consisting  virtually  of  one  or  more  irregular  pulmonary  cavi- 
ties, with  smooth  linings  and  thick  fibrous  walls — the  so-called 
"trabecular  bronchiectasis."  Sometimes,  despite  extensive  distri- 
bution of  the  lesions,  there  is  but  a  scanty  secretion  within  the 
bronchi;  but  ordinarily  the  dilated  portions  are  filled  with 
mucopurulent  material,  swarming  with  bacteria  and  containing 
desquamated  epithelium,  and  perhaps  erythrocytes  and  bits  of 
necrotic  tissue,  from  the  decomposition  of  which  elements  arises  an 
intolerable  fetor.  Away  from  the  seat  of  the  dilatation  the  bronchi 
show,  in  variable  degree,  the  changes  of  chronic  bronchitis.  In  the 
neighborhood  of  a  bronchiectatic  lesion  pleural  adhesions  and  thick- 
ening commonly  exist,  and  the  lung  may  show  patches  of  compression 
atelectasis,  fibrosis,  lobular  consolidation,  and  emphysema.  Pul- 
monary abscess  and  gangrene,  purulent  pleurisy,  peritonitis,  and 
cerebral  abscess  are  other  complications  occasionally  traceable  to 
infection  from  the  bronchiectatic  secretion.  Hypertrophic  pulmo- 
nary osteo-arthropathy  develops  in  certain  cases  of  bronchiectasis, 
as  the  result,  so  Marie  believes,  of  irritation  of  the  osseous  structures 
by  toxins  evolved  in,  and  absorbed  from,  the  bronchial  lesions. 

Physical  Signs. — In  a  considerable  proportion  of  cases  no  definite 
physical  signs  are  demonstrable,  owing  .to  the  small  size  and  deep 
situation  of  the  lesions  and  to  the  abundance  of  their  contained  secre- 
tion. Relatively  large,  empty  ectases  near  the  surface  (or,  if  deep 
seated,  surrounded  by  consolidated  lung)  afford  the  signs  of  a  pul- 
monary cavity,  more  frequently  basal  than  apical. 

Inspection. — The  subject  of  extensive  bronchiectasis  may  show 
no  traces  of  such  a  condition,  or  he  may  breathe  laboriously,  appear 
cyanotic,  become  emaciated,  and  wear  the  hectic  facies  of  septic 
poisoning.  The  signs  of  Marie's  disease  (enlargement  of  the  hands 
and  feet  with  bulbous  clubbing  of  the  terminal  phalanges)  should 
be  carefully  looked  for  in  all  cases  of  suspected  bronchial  dilatation. 


j82  PHYSICAL    DIAGNOSIS 

The  thorax,  if  at  all  abnormal,  shows  areas  of  deficient  expansion, 
contraction,  and  emphysematous  enlargement,  with  corresponding 
alterations  in  the  respiratory  excursion  over  these  parts.  The 
fluoroscope  may  reveal  the  site  of  the  dilatation,  a  well-defined  opacity 
being  produced  by  an  empty  cavity,  and  a  dark,  circumscribed 
shadow  by  one  filled  with  secretion. 

Palpation,  Percussion,  and  Auscultation. — Over  an  accessible 
empty  bronchiectatic  cavity  one  expects  to  find  increased  vocal 
fremitus,  a  tympanitic  (perhaps  "cracked  pot")  percussion  sound, 
bronchophony  which  may  amount  to  clean-cut  whispering  pectoril- 
oquy,  cavernous  or  amphoric  breath-sounds,  and  moist  cavernous 
rales  or  gurgles.  With  more  or  less  constancy  it  is  also  possible 
to  demonstrate  the  various  special  tonal  changes  of  the  percussion 
sound  indicative  of  a  cavity.  (See  p.  144.)  The  foregoing  signs, 
however,  disappear  when  the  dilatation  becomes  filled  with  secretion 
or  when  the  communicating  bronchus  becomes  obstructed,  but  they 
reappear  when  the  cavity  is  emptied  and  the  tube  cleared,  as  by  a 
paroxysm  of  coughing.  The  tendency  of  the  physical  signs  thus 
to  come  and  go  is  most  suggestive  of  a  bronchiectatic  cavity.  Aside 
from  the  purely  cavernous  signs,  those  relating  to  coexisting  bron- 
chitis, emphysema,  and  pleuropulmonary  fibrosis  are  commonly 
ingrafted  upon  the  clinical  picture,  and,  indeed,  it  is  not  at  all  unusual 
for  such  findings  to  predominate.  In  some  instances  the  heart  is 
dislocated,  by  traction,  toward  the  site  of  the  dilatation. 

Diagnosis. — Bronchiectasis  is  suggested  by  a  history  of  chronic 
bronchitis  or  of  a  fibroid  lung  or  pleura  in  a  person  who  tells  of  the 
periodic  and  copious  expectoration  of  foul-smelling  mucopurulent 
sputum.  After  standing  in  a  conic  vessel,  such  sputum  separates 
into  two  strata,  the  lower  consisting  of  a  granular  sediment  of  pus, 
de'bris,  fatty  acids,  and  hematoidin  crystals,  and  the  upper  of  a  thin, 
mucoid  liquid  overlaid  by  dirty  froth.  With  a  history  of  this  sort, 
the  diagnosis  is  confirmed  by  the  demonstration  of  a  basal  cavity 
whose  special  physical  signs  are  influenced  by  cough,  expectoration, 
and  posture,  but  which  do  not  alter  perceptibly  so  as  to  denote  pro- 
gressive increase  in  the  size  of  the  original  excavation,  even  after  the 
lapse  of  a  considerable  period. 

Fetid  bronchitis  and  bronchiectasis  require  differentiation,  since  in 
both  affections  the  patient  may  expectorate  large  quantities  of  evil- 
smelling,  purulent  material.  In  questionable  cases  the  detection 
of  a  basal  cavity  is  conclusive,  but  the  presence  of  wide-spread  bron- 
chi tic  signs  is  merely  suggestive — small,  deeply  seated  bronchiectases 
(which  perhaps  are  part  and  parcel  of  a  putrid  bronchitis)  defy 


DISEASES   OF   THE    BRONCHOPULMONARY   SYSTEM          183 

recognition,  at  least  with  any  degree  of  certainty.     It  is  sometime 
of  use  to  remember  that  in  bronchiectasis  there  is  more  likelihood 
of  severe  constitutional  symptoms  and  of  "evacuative"  cough  and 
expectoration,  while  in  fetid  bronchitis  the  expectoration  is  practically 
continuous. 

Empyema  with  a  fistulous  bronchial  outlet  sometimes  accounts  for 
the  sudden  expectoration  of  a  mouthful  of  foul,  purulent  matter,  but 
here  there  are  unmistakable  physical  signs  of  a  pleural  effusion,  and 
also  a  helpful  case-history. 

If  pulmonary  actinomycosis  be  suspected,  owing  to  the  fetor  of  the 
sputum,  the  latter  should  be  examined  microscopically  for  character- 
istic ray-fungus  granules.  The  physical  signs  of  bronchiectatic 
and  pulmonary  cavities  are  discussed  under  Phthisis,  Pulmonary 
Abscess,  and  Pulmonary  Gangrene.  (See  pp.  218,  256,  and  259.) 

BRONCHOSTENOSIS    (Stenosis  of  the  Bronchi;  Bronchiarctia) 

Clinical  Pathology. — Narrowing  or  stricture  of  the  bronchial 
lumen  depends  upon  numerous  factors  relating  either  to  obstruction 
within,  or  to  external  pressure  upon,  the  tubes.  In  the  former  class 
of  causes  are  included  swelling  of  the  bronchial  mucosa,  fibrinous 
and  membranous  plugs,  foreign  bodies,  broncholiths,  neoplasms, 
tuberculous  lesions,  and  syphilitic  cicatrices.  To  the  latter  group 
belong  factors  such  as  tracheobronchial  adenitis,  pleuropulmonary 
fibrosis,  solid  tumors,  cysts,  and  abscesses  of  the  mediastinum, 
aneurism  of  the  thoracic  aorta,  large  pleural  and  pericardial  effusions, 
and  extreme  dilatation  of  the  left  auricle. 

According  to  the  character  of  the  underlying  cause,  bronchial 
stenoses  are  attended  by  more  or  less  bronchitis,  by  local  necrosis 
and  ulceration,  and  by  inflammation  of  the  peribronchial  structures. 
When  a  bronchus  of  some  size  is  completely  occluded,  the  pulmonary 
structure  supplied  by  the  stenotic  tube  is  rapidly  deprived  of  air  by 
absorption,  and  in  consequence  the  airless  portion  of  the  lung  relaxes, 
and  sooner  or  later  collapses,  this  change  being  termed  obturation 
atelectasis.  In  some  instances  the  obstruction  virtually  serves  as  a 
ball- valve,  allowing  no  air  to  enter  the  lung  during  inspiration,  but  not 
interfering  with  its  egress  during  expiration.  The  clinical  features  of 
bronchial  stenosis  vary  greatly  with  the  character,  degree,  and  site 
of  the  constriction,  and,  hence,  with  the  nature  of  its  bronchopul- 
monary  sequelae,  especially  those  affecting  the  distal  portion  of  the 
lung.  If  a  primary  bronchus  be  obstructed,  the  entire  lung  of  the 
same  side  is  crippled;  if  a  smaller  sized  tube  be  blocked,  the  circum- 


1 84 


PHYSICAL   DIAGNOSIS 


scribed  patch  of  the  lung  beyond  is  affected;  while  in  bronchiolar 
stenosis,  unless  it  be  very  extensive,  the  resulting  lobular  airlessness 
is  usually  masked  by  the  emphysema tous  condition  of  the  surrounding 
pulmonary  tissue. 

Physical  Signs. — On  inspection  there  is  obvious  dyspnea,  prin- 
cipally of  the  inspiratory  type,  ranging  in  intensity  from  moderate 
shortness  of  breath  to  extreme  orthopnea  with  cyanosis.  The  respi- 
ratory movements  are  hurried,  restricted,  and  inadequate,  especially 
on  the  affected  side,  and  they  cause  overaction  of  the  auxiliary 
muscles  of  breathing.  Inspiratory  retraction  of  the  lower  ribs  and 
interspaces  on  the  side  of  the  lesion  is  observed  in  case  the  residual 
air  is  notably  exhausted  and  rarefied.  Blocking  of  a  large  bronchus 
tends  to  provoke  vicarious  exaggeration  of  the  thoracic  movements 
on  the  opposite  side.  The  foregoing  signs  are  usually  accompanied 
by  paroxysmal  cough,  either  dry  and  hard,  or  productive  of  sputum 
of  variable  amount  and  composition.  Palpation  reveals  enfeebled 
or  abolished  vocal  fremitus  over  the  lung  lying  peripheral  to  the 
obstruction,  which  interferes  with,  or  entirely  damps,  the  trans- 
mission of  the  voice  vibrations.  Furthermore,  the  coexistence 
of  vesicular  dilatation  in  the  neighboring  pulmonary  structure 
is  an  associated  factor  of  diminished  tactile  fremitus.  Percussion 
gives  no  noteworthy  findings,  save  in  the  event  of  atelectasis  or  of 
wide-spread  emphysema,  which  may  yield,  respectively,  dulness 
or  hyperresonance.  It  sometimes  happens  that  the  normal  inspir- 
atory exaggeration  of  the  percussion  sound  is  ill  defined,  if  not  quite 
imperceptible.  On  auscultation  loud  sibilant  and  sonorous  rales  and 
numerous  mucous  sounds  generated  in  the  bronchial  exudate  are 
audible  at  the  site  of  the  constriction,  while  over  the  lung  beyond 
the  latter  the  respiratory  murmur  and  vocal  resonance  are  enfeebled 
or  abolished. 

Diagnosis. — The  association  of  inspiratory  dyspnea  and  cough 
with  circumscribed  bronchial  rales  and  a  patch  of  airless  lung  indi- 
cates bronchial  stenosis,  the  character  of  which  is  to  be  determined 
by  finding  the  exciting  cause  of  the  lesion  in  the  instance  in  question. 
Laryngeal  obstruction,  directly  diagnosed  by  laryngoscopy,  is  accom- 
panied by  hoarseness,  urgent  dyspnea,  harsh,  stridulous  breath- 
sounds,  and  unnaturally  extensive  movements  of  the  larynx  during 
respiration.  Tracheal  obstruction,  which  does  not  distinctly  alter 
the  voice,  may  also  provoke  stridor,  and  is  commonly  attended  by 
orthopnea  and  by  limited  movements  of  the  larynx. 


DISEASES  OF  THE   BRONCHOPULMONARY   SYSTEM          185 

PULMONARY   CONGESTION   (Hyperemia  of  the  Langs) 

Clinical  Pathology. — Acute  or  active  congestion  of  the  lungs  is 
characterized  by  an  intense  engorgement  of  the  pulmonary  capillaries, 
commonly  of  both  lungs,  attended  by  the  accumulation  of  blood- 
serum  within  the  air-vesicles  and  by  more  or  less  swelling  and  shedding 
of  their  epithelium.  A  lung  thus  affected  is  larger,  firmer,  and  less 
resilient  than  normal,  of  a  dark-red  color,  and  deficient  in,  though 
not  wholly  deprived  of,  air;  it  pits  on  pressure,  and  on  section  yields 


Blood-clots  in 
bronchi 

Area  of  inflammatory 
consolidation 


Congested  area 


Fig-  94- — Pulmonary  congestion  (Jefferson  Hospital  Laboratories). 

a  considerable  amount  of  bloody  serum.  Since  acute  pulmonary 
congestion  commonly  leads  to  exudative  inflammation,  of  which  it 
is,  in  reality,  the  first  stage,  and  also  tends  to  set  up  transudative 
processes,  it  is  impossible  always  to  recognize  any  clearly  defined 
distinctions  between  these  conditions.  Such  a  condition  of  "active 
fluxion,"  typified  by  the  stage  of  engorgement  in  an  extensive  croup- 
ous  pneumonia,  may  be  excited  by  exposure  to  extremes  of  heat 
and  cold,  by  the  inhalation  of  irritating  vapors,  by  violent  exercise, 


PHYSICAL   DIAGNOSIS 

and  by  toxemia  due  to  the  presence  of  poisonous  substances  in  the 
blood;  congestion  doubtless  also  exists  in  the  pulmonary  types  of 
vicarious  menstruation.  Woillez's  disease,  or  the  "acute  idiopathic 
pulmonary  congestion"  of  the  French  school,  is  probably  nothing 
but  an  abortive  form  of  pneumonia,  terminating  before  the  stage  of 
consolidation.  Collateral  congestion  or  fluxion  is  a  form  of  hyper- 
emia  affecting  portions  of  the  lung  adjacent  to  some  local  pulmonary 
lesion,  as  in  infarction,  pneumonia,  phthisis,  and  bronchitis.  It 
arises  in  consequence  of  a  local  circulatory  disturbance,  and  impli- 
cates, to  a  greater  or  less  extent,  the  pulmonary  structure  not  pri- 
marily diseased. 

Chronic  or  passive  congestion  of  the  lungs  develops  as  the  result  of 
habitual  stasis  of  the  pulmonary  circulation  due  to  various  conditions 
mechanically  interfering  with  the  return  of  blood  to  the  heart,  or 
enfeebling  the  cardiac  force.  Meclianical  congestion,  ultimately 
leading  to  a  change  in  the  pulmonary  parenchyma  known  as  brown 
induration,  is  a  common  sequel  of  valvular  and  mural  disease  of  the 
left  heart.  When  thus  affected,  the  lungs  are  the  seat  of  permanent 
fibrosis  and  pigmentation,  being  abnormally  large,  unduly  firm,  and 
of  a  dark-brown  color.  The  connective  and  elastic  tissues  are 
increased,  the  capillaries  are  distended  and  tortuous,  and  the  air- 
vesicles  contain  a  catarrhal  exudate  filled  with  desquamated  alveolar 
epithelium  and  leukocytes  studded  with  pigment-granules.  The 
extensive  pigmentation,  so  characteristic  of  this  type  of  chronic 
congestion,  is  due  to  hemolysis  which  causes  erythrocytic  disintegra- 
tion, some  of  the  blood-pigment  thereby  liberated  being  ingulfed 
by  the  alveolar  epithelium  and  by  leukocytes  and  removed  by  expec- 
toration, while  other  particles  are  deposited,  via  the  lymph-channels, 
in  the  pulmonary  parenchyma. 

Hypostatic  congestion,  affecting  the  dependent  parts  of  the  lungs, 
is  referable  to  a  feeble  heart  plus  the  effect  of  gravity  and  deficient 
expansion  of  the  pulmonary  tissue.  It  occurs  with  frequency  in 
various  febrile  and  asthenic  conditions  that  necessitate  prolonged 
recumbency,  and  in  such  states  it  shows  a  special  predilection  for  the 
bases  posteriorly.  It  may  also  attend  lesions  of  the  brain,  morphin- 
poisoning,  and  comatose  states  in  general,  and  the  bases  of  the  lung 
may  show  this  sort  of  congestion  as  a  consequence  of  pressure  exerted 
by  intra-abdominal  effusions  and  tumors.  Hypostatic  congestion 
is  more  active  a  process  than  the  mechanical  form,  and,  unlike  it, 
does  not  set  up  a  fibrous  overgrowth.  The  air-vesicles  are  choked 
with  blood-cells  and  the  products  of  their  destruction  and  with 
desquamated  epithelium  and  serum.  The  congested  areas  are  boggy 


DISEASES   OF   THE    BRONCHOPULMONARY    SYSTEM          187 

with  blood,  abnormally  heavy,  practically  airless,  and  dark  red  or 
even  black-red  in  color,  resembling,  in  the  extreme  example,  the  tissue 
of  the  spleen — hence  the  expression,  pulmonary  splenization,  commonly 
applied  to  this  change.  Should  edema  and  inflammation  be  ingrafted 
upon  this  primary  engorgement,  a  state  of  hypostatic  pneumonia 
is  said  to  exist. 

Physical  Signs. — Acute  Congestion. — The  physical  signs  naturally 
vary  with  the  intensity  and  distribution  of  the  process,  as  well  as 
with  the  presence  or  absence  of  coexisting  edema  and  inflammation 
in  and  near  the  congested  area.  If  the  fluxion  be  circumscribed, 
the  evidences  are  much  clearer,  by  comparison  with  the  healthy  lung, 
than  if  it  be  widely  disseminated. 

Inspection  ordinarily  shows  either  a  flushed  face  or  cyanosis,  dysp- 
nea, polypnea,  restricted  respiratory  movements,  cough,  and  perhaps 
hemoptysis,  should  the  engorgement  be  very  intense.  On  palpation, 
the  vocal  fremitus,  if  altered  at  all,  is  found  to  be  moderately  increased. 
The  percussion  sound  is  of  higher  pitch  than  normal,  and  the  resistance 
to  the  pleximeter  finger  is  somewhat  exaggerated;  or  the  defective 
resonance  may  still  more  closely  approach  actual  dulness.  Auscul- 
tation reveals  either  suppressed,  feeble  breath-sounds,  or  a  harsh 
respiratory  murmur,  whose  expiratory  phase  is  comparatively  high- 
pitched,  prolonged,  and  blowing.  Fine  crepitant  rales  are  audible 
when  the  vesicles  contain  serum. 

Chronic  Congestion. — In  chronic  congestion  of  the  mechanical 
type  the  most  striking  signs  commonly  relate  to  the  underlying  cardiac 
defect,  which  in  most  instances  consists  primarily  of  mitral  stenosis, 
regurgitation,  or  both,  later  succeeded  by  right  ventricular  enlarge- 
ment. 

Inspection  shows,  apart  from  the  cardiac  findings,  habitual  and 
distressing  dyspnea,  which  in  time  becomes  true  orthopnea,  with 
decided  cyanosis  and  a  variable  degree  of  anasarca.  The  respira- 
tory excursions,  which  are  hurried,  are  notably  freer  at  the  apex 
than  at  the  base  of  the  lungs.  There  is  cough,  productive  of  con- 
siderable thin  sputum,  often  frothy  and  blood-streaked,  and  charged 
with  blood-pigment,  both  free  and  contained  within  alveolar  epithelial 
cells — the  so-called  "heart-disease  cells."  Palpation  over  the  bases 
gives  tactile  fremitus  of  varying  grades — feeble,  in  a  simple  passive 
congestion,  and  increased,  if  much  fibrosis  has  developed.  Percus- 
sion elicits  basal  dulness,  and  above  it  a  generally  hyperresonant 
sound  is  frequently  distinguishable.  On  auscultation,  enfeebled, 
harsh,  or  even  bronchial  breathing  is  audible,  according  to  the  degree 
of  congestion  and  attendant  changes  existing  in  the  individual  case. 


1 88  PHYSICAL   DIAGNOSIS 

Simple  congestion  tends  to  obscure  the  breath -sounds,  while  dense  in- 
duration of  the  lung  intensifies  them.  Crepitations  indicate  the  pres- 
ence of  intra vesicular  fluid.  In  hypostatic  congestion  the  requisite  con- 
ditions usually  exist  to  bronchialize  the  respiratory  murmur,  to  impair 
resonance,  and  to  cause  mucous  bubbling  at  the  bases,  but  in  dealing 
with  this  condition  one  also  must  always  search  for  physical  signs  due 
to  associated  edema  and  to  pneumonia. 

Diagnosis. — In  detecting  a  pulmonary  congestion  the  patient's 
history  gives  fully  as  important  data  as  the  physical  signs,  so  that 
in  every  suspected  case  a  thorough  inquiry  should  be  made  for  some 
primary  factor  capable  of  surcharging  the  lungs  with  blood,  either 
by  precipitating  an  active  fluxion,  or  by  impeding  the  return  flow 
of  blood  to  the  left  heart.  This  question  having  been  decided,  it 
is  not  difficult  to  interpret  correctly  the  significance  of  dyspnea, 
cyanosis,  cough,  and  frothy,  bloody  sputum,  accompanied  by  basal 
signs  of  deficient  aeration  and  incomplete  consolidation.  Conges- 
tion of  the  lungs  versus  croupous  pneumonia,  is  considered  in  connection 
with  this  infection.  (See  p.  211.) 

PULMONARY  EDEMA  (Pulmonary  Dropsy?  Serous  Infiltration  of  the 
Lung;  Serous  Apoplexy  of  the  Lung;  Pneumochysis) 

Clinical  Pathology. — In  pulmonary  edema  the  air-vesicles,  their 
walls,  and  their  communicating  bronchioles  are  flooded  with  a  serous 
or  a  serosanguinolent  transudate,  and  in  consequence  of  this  dropsical 
condition  the  affected  tissue  becomes  partly  deprived  of  air,  swollen, 
boggy,  and  pale.  On  section,  the  cut  surface  exudes  a  thin,  frothy 
fluid,  clear  or  tinged  with  blood,  and  containing  a  variable  number 
of  blood-corpuscles,  alveolar  epithelial  cells,  and  pigment-granules. 
When  edema  is  associated  with  congestion,  as  so  often  is  the  case, 
hyperemic  discoloration  is  apparent,  and  when  consolidation  coexists, 
the  lung  is  of  a  gelatinous  consistence  and  appearance.  The  bronchi 
contain  thin,  frothy,  blood-tinged  or  decidedly  hemorrhagic  fluid,  and 
the  peribronchial  lymphatic  glands  are  in  some  instances  preter- 
naturally  soft.  Unless  inflammatory  complications  are  also  present, 
the  pleural  surfaces  show  no  noteworthy  changes.  Pulmonary 
edema,  which  may  be  either  general  or  local,  ordinarily  implicates 
the  lower  lobes.  Coplin,  in  a  study  of  2030  autopsies,  found  the 
lungs  edematous  in  20  per  cent.,  the  process  being  unilateral  in  9 
per  cent.,  and  affecting  the  right  lung  a  shade  more  frequently  than 
the  left.  When  circumscribed  to  the  neighborhood  of  a  pneumonic 
or  other  inflammatory  lesion  of  the  lung,  an  edema  is  designated  as 


DISEASES   OF   THE    BRONCHOPULMONARY   SYSTEM          189 

collateral,  focal,  or  inflammatory.  As  the  result  of  passive  pulmonary 
hyperemia  congestive  edema  is  prone  to  develop  in  the  dependent 
portions  of  the  lungs.  An  acute  fulminating  edema  of  the  lungs  and 
bronchi  is  occasionally  met  with,  especially  in  conditions  of  arterial 
and  renal  sclerosis,  the  edematous  changes  being  attended  by  intense 
diffuse  engorgement  and  by  a  copious  outpouring  of  richly  albuminous 
fluid  containing  numerous  leukocytes.  Vasomotor  disturbances 
linked  with  a  disproportionately  forcible  action  of  the  right  ventricle 
is  supposed  to  excite  this  type  of  edema,  which  may  rapidly  cause 
death,  though  it  sometimes  recurs  repeatedly  in  the  same  individual. 
The  apparent  determining  factors  of  pulmonary  edema  are  hyper- 
tension of  the  pulmonary  circulation,  plus  a  relative  weakness  of 
the  left  ventricle,  together  with  a  hydremic  blood-mass  and  undue 
permeability  of  the  capillary  walls.  Sudden  vasomotor  paresis  also 
is  a  plausible  explanation  in  some  instances. 

General  edema  and  congestion  of  the  lungs  are  frequently  associated 
conditions,  and  have  numerous  factors  in  common — sepsis,  toxemia, 
cardiac  failure,  exposure,  and  irritation  of  the  bronchopulmonary 
mucosa.  Edema  is  to  be  looked  for  as  the  terminal  event  in  many 
illnesses,  notably  in  nephritis,  cardiac  affections,  grave  anemias, 
cerebral  diseases,  acute  infections,  and  cachectic  states.  It  develops 
collaterally  in  connection  with  many  cases  of  pneumonia,  phthisis, 
abscess,  and  infarction  of  the  lungs.  Exceptionally,  pulmonary 
edema  is  an  embarrassing  sequel  to  etherization  and  to  thoracentesis, 
as  well  as  a  complication  of  angioneurotic  edema  of  the  surface  of 
the  body. 

Physical  Signs. — Inspection  shows  dyspnea,  cyanosis,  and  restric- 
tion of  the  respiratory  excursions  of  a  degree  commensurate  with  the 
extent  of  the  edema  and  the  character  of  its  primary  cause.  There 
is  cough,  often  painful,  and  productive  of  copious  gushes  of  frothy, 
thin,  serous  or  blood-tinged  fluid.  Ordinarily,  unless  some  essen- 
tially febrile  disease  coexists,  there  are  no  signs  of  fever.  Palpation 
over  the  water-logged,  inelastic  lung  detects  little  or  no  vocal  fremitus, 
while  above  it  rhonchal  vibrations  are  commonly  felt.  With  the 
onset  of  an  acute  edema  the  pulse  is  full,  bounding,  and  of  extra- 
ordinarily high  tension,  but  later  this  gives  way  to  feebleness,  arhyth- 
mia,  and  virtual  pulselessness.  Percussion  yields  dulness  and 
increased  resistance  over  the  dropsical  area,  with  progressive  upward 
extension  of  the  impaired  resonance  as  the  process  spreads.  In 
exceptional  cases  of  fulminating  edema,  however,  the  presence  of 
extensive  lobular  overdistention  and  of  bronchial  paralysis  may 
cause  general  hyperresonance,  despite  the  flooded  vesicles — the  so- 


I  go  PHYSICAL   DIAGNOSIS 

called  paradoxic  percussion  sound  of  Huchard.  Auscultation  detects 
enfeebled  respiratory  and  voice  sounds,  and  numerous  fine  moist 
rales  over  the  dependent  parts  of  the  lungs.  These  rales,  of  vesicular 
and  bronchiolar  origin,  have  a  distinctive  liquid  quality,  and  are 
diffused,  "like  a  rising  tide,"  through  the  lungs  as  the  edema  spreads. 
They  are  masked  by  intense,  coarse,  liquid  bubbling  sounds  when 
the  larger  bronchi  fill  with  the  transudate. 

Diagnosis. — Having  found  some  adequate  determining  cause, 
the  association  of  basal  dulness,  suppressed  respiratory  sounds,  and 
distinctively  liquid  rales,  with  labored  breathing,  cough,  and  abun- 
dant serous  expectoration,  is  good  evidence  of  pulmonary  edema. 
A  terminal  edema,  it  should  be  recalled,  may  develop  stealthily,  with 
few,  if  any,  clinical  phenomena  save  those  obtained  by  percussion 
and  auscultation.  Acute  fulminating  edema  provokes  alarming 
dyspnea  and  cyanosis,  and  is  likely  to  arise  without  warning  or  obvious 
cause,  in  persons  apparently  in  good  health,  the  symptoms  resemb- 
ling, at  least  superficially,  pulmonary  infarction,  acute  bronchial 
spasm,  and  certain  inflammatory  processes  of  the  lungs  and  pleurae. 

Bronchial  asthma,  like  acute  pulmonary  edema,  is  paroxysmal, 
recurrent,  prone  to  be  nocturnal,  and  attended  by  dyspnea  and 
cough,  but  in  asthma  the  patient  usually  has  an  accurate  premonition 
of  the  attack,  which  supervenes  progressively,  and  gives  a  history  of 
long-standing  bronchitis  and  emphysema,  while  the  physical  signs 
relate  to  a  characteristic  type  of  expiratory  dyspnea,  to  scanty,  viscid 
expectoration  charged  with  Curschmann's  spirals,  to  general  thoracic 
hyperresonance,  and  to  a  predominance  of  dry  bronchial  rales. 

The  differentiation  of  acute  edema  of  the  lungs  from  infarction, 
pneumonia,  and  pleurisy  is  detailed  under  these  last-named  subjects. 
(See  pp.  192,  198,  and  268.) 

PULMONARY  HEMORRHAGIC  INFARCTION  (Pulmonary  Apoplexy; 
Pneumorrhagia;  Embolic  Pneumonia) 

Clinical  Pathology. — When  an  embolus  or  a  thrombus  plugs  a 
terminal  branch  of  the  pulmonary  artery  and  the  resulting  anastomo- 
sis is  insufficient  adequately  to  carry  on  the  circulation,  extravasation 
of  blood  takes  place  into  the  neighboring  air-cells  and  their  septa, 
thereby  producing  the  pulmonary  lesion  known  as  hemorrhagic 
infarction.  The  obstructing  emboli  are  commonly  derived  from 
clots  lodged  within  the  right  heart,  which  has  become  dilated  and 
thrombotic  as  a  consequence  of  mitral  obstruction,  or  from  clots 
within  one  of  the  systemic  veins;  in  certain  instances  pulmonary 


DISEASES   OF   THE    BRONCHOPULMONARY    SYSTEM          IQI 

artery  thrombosis  has  been  found  to  be  the  exciting  cause  of  an 
infarct.  The  area  of  infarction  is  usually  of  pyramidal  shape,  with 
well-defined  margins  and  base  directed  toward  the  periphery  of  the 
lung;  such  patches  may  be  either  single  or  multiple,  and  their  size 
ranges  from  a  few  centimeters  in  the  longest  axis  to  an  extravasation 
diffused  through  virtually  an  entire  lobe  (Fig.  95).  Recent  infarcts 
are  dense,  firm,  almost  airless,  and  of  dark-red  color,  which  in  time 
changes  to  a  dingy  brown  hue.  Microscopically,  the  air-vesicles 
and  bronchioles  are  gorged  with  blood-cells  and  the  intervesicular 
walls  infiltrated  with  the  same  elements.  The  pleura  bordering 


Infarcted  area 


Infarcted  area 
Fig-  95- — Pulmonary  infarction  (Jefferson  Hospital  Laboratories). 

upon  the  infarction  rarely  escapes  plastic  inflammation,  and  may 
exude  a  copious  effusion  into  the  pleural  sac,  while  the  adjacent  lung 
shows  a  variable  degree  of  congestion  and  edema,  if  not,  indeed, 
pneumonic  changes.  An  uncomplicated  sterile  infarct,  after  absorp- 
tion of  the  effused  blood  has  occurred,  generally  leaves  a  brownish 
or  slate-colored  scar,  though  it  is  not  impossible  for  the  affected 
area  to  become  entirely  restored,  leaving  no  visible  trace  of  the  infarc- 
tion. A  septic  infarct  may  be  the  starting-point  of  abscess  or  of 
gangrene,  which  latter  is  capable  of  fistulating  into  the  pleural  cavity 
and  establishing  a  pneumothorax. 


1 92  PHYSICAL    DIAGNOSIS 

Physical  Signs. — The  physical  signs  of  pulmonary  infarction 
are  substantially  those  of  a  compact  local  consolidation  modified 
by  concurrent  congestion,  edema,  and  pneumonia,  and  in  the  in- 
dividual case  they  vary  according  to  the  size,  number,  and  situa- 
tion of  the  infarcted  areas  and  the  circulatory  derangements  thereby 
produced.  In  general,  it  may  be  stated  that  an  infarct  must  have 
a  peripheral  extent  of  at  least  five  square  centimeters  to  afford 
definite  percussion  and  auscultatory  data,  and  that  in  central  infarc- 
tions examination  of  the  chest  gives  no  certain  information.  On 
inspection  there  is  more  or  less  labored,  painful,  and  hurried  respira- 
tion with  cough  and  hemoptysis,  while,  exceptionally,  syncope  and 
convulsions  attend  the  development  of  an  extensive  infarction.  If 
sterile,  the  latter  is  usually  not  associated  with  fever,  but  if  infected, 
the  familiar  objective  symptoms  of  sepsis  ensue.  Palpation,  per- 
cussion, and  auscultation  afford,  in  typical  examples,  exaggerated 
vocal  fremitus,  dulness,  bronchial  breathing,  bronchophony,  pleural 
friction,  and  numerous  crepitant  and  subcrepitant  rales  over  a  sharply 
defined  circumscribed  area  commonly  situated  posteriorly  over  a 
lower  lobe.  These  signs,  even  though  no  inflammatory  complications 
exist,  are  subject  to  material  modifications,  due  chiefly  to  the  damp- 
ing of  voice  vibrations  by  flooded  bronchi,  and  to  the  masking  of 
crepitations  by  loud  rales. 

Diagnosis. — In  a  patient  suffering  from  mitral  disease  or  other 
lesion  from  which  emboli  may  be  derived,  the  abrupt  onset,  without 
fever,  of  acute  respiratory  embarrassment,  sharp  pleural  pain, 
bloody  expectoration,  and  the  physical  signs  of  a  clearly  delimited 
patch  of  pulmonary  solidification  are  sufficient  for  the  diagnosis. 
Infarctions  due  to  septic  emboli  are  recognized  primarily  by  similar 
signs,  and  later  by  those  relating  to  abscess  or  gangrene  of  the  lung, 
as  well  as  by  the  "pump-handle"  temperature,  recurrent  rigors, 
sweats,  and  rapid  emaciation  accompanying  these  grave  affections. 
Small  deep-seated  infarctions,  be  they  single  or  multiple,  rarely  give 
rise  to  anything  more  definite  than  dyspnea,  cough,  and  moderate 
hemoptysis.  The  distinctions  between  infarction  of  the  lung  and 
croupous  pneumonia  are  given  under  the  latter  infection.  (See  p.  198.) 

CATARRHAL   PNEUMONIA    (Bronchopneumonia;    Lobular,    Dissemi- 
nated, or  Peribronchial  Pneumonia;  Suffocative  Catarrh) 

Clinical  Pathology. — Catarrhal  pneumonia  is  primarily  an  inflam- 
mation of  the  bronchioles  and  alveoli  of  the  pulmonary  lobules, 
leading  to  their  partial  or  complete  consolidation  and  to  consecutive 


DISEASES   OF   THE   BRONCHOPULMONARY   SYSTEM 


193 


hyperemia,  collapse,  and  overdistention  of  the  neighboring  vesicular 
structures  (Fig.  96).  If  the  bronchopneumonic  process  be  widely 
disseminated,  involving  the  fusion  of  multiple  lobular  lesions,  an 
entire  lobe  may  be  converted  into  an  almost  airless  mass  of  solidifica- 
tion. Almost  invariably  the  initial  lesion  consists  of  inflammation 
of  the  terminal  bronchioles,  which  rapidly  invades  the  corresponding 
vesicles  of  the  bronchiolar  territory;  in  exceptional  instances  only 


Pneumonic  infiltration 


Site  of  aorta 


Exudate  in  bronchi 


Thickened  pleura 


Diaphragm 
Fig.  96. — Catarrhal  pneumonia  (Jefferson  Hospital  Laboratories). 

does  the  inflammation  first  arise  within  the  vesicles,  from  primary 
disease  of  the  septa.  No  special  microorganism  of  catarrhal  pneu- 
monia has  been  isolated,  and  the  disease  may  be  excited  by  numerous 
varieties  of  bacteria,  such  as  the  pneumococcus,  streptococcus, 
staphylococcus,  pneumobacillus,  and  the  bacilli  of  influenza,  diph- 
theria, leprosy,  and  tuberculosis,  the  resulting  infection  being  far 
more  frequently  mixed  than  pure. 

The  lung  of  catarrhal  pneumonia  varies  considerably  in  gross 
13 


194  PHYSICAL    DIAGNOSIS 

appearance,  according  to  the  acuteness  and  distribution  of  the  bron- 
chiolar  and  vesicular  changes.  Taking  a  well-marked  acute  case 
as  an  illustration,  the  organ,  as  a  whole,  is  swollen,  lacks  resiliency, 
is  unduly  resistant  (though  not  wholly  deprived  of  air),  and  has  a 
curiously  mottled  appearance,  due  to  the  presence  of  consolidative, 
congestive,  collapsed,  and  overdistended  areas.  The  bronchopneu- 
monic  patches  consist  of  red,  non-crepitant,  firm,  nodular  masses, 
surrounded  by  a  hyperemic  zone,  these  areas,  as  resolution  ensues, 
turning  gray  and  undergoing  softening  and  absorption,  with  ulti- 
mate restoration  of  the  inflamed  foci.  Purple  spots  of  atelectasis, 
usually  sunk  below  the  surface  of  the  lung,  are  particularly  numerous 
at  the  base,  although  these  evidences  of  lobular  collapse  may  also 
be  thickly  distributed  through  the  greater  part  of  a  lobe.  Pale 
zones  of  emphysema  impinge  upon  the  pneumonic  patches,  and  also 
affect  the  upper  portions  and  the  anterior  borders  of  the  lungs.  On 
cross-section  through  a  lobule  three  characteristic  zones  are  dis- 
tinguishable, from  within  outward:  the  central  distended  bronchiole, 
choked  with  viscid  mucopurulent  material;  a  middle  zone  of  vesic- 
ular consolidation,  at  first  presenting  a  red  or  grayish-red,  dense 
surface,  which  is  more  commonly  smooth  than  granular,  but  later 
becoming  paler,  softer,  and  stippled  with  small  purulent  areas; 
and  an  outer  zone  of  atelectasis,  composed  of  collapsed,  airless 
vesicular  tissue,  matted  together  by  low-grade  inflammation.  Under 
the  microscope  the  air-vesicles  and  bronchioles  are  found  to  be  dis- 
tended with  an  exudate,  wholly  or  almost  devoid  of  fibrin,  and  rich 
in  desquamated  epithelium,  leukocytes,  and  bacteria,  with  but  few, 
if  any,  erythrocytes.  Leukocytic  infiltration  of  the  alveolar  septa 
and  the  walls  of  the  terminal  tubes  is  present  to  a  greater  or  less 
degree.  If  resolution  progresses  favorably,  the  inflammatory  pro- 
ducts soften  and  are  disposed  of  by  expectoration  and  resorption, 
and  restoration  of  the  epithelial  surfaces  takes  place.  If  resolution 
be  defective  and  infection  ensues,  tuberculosis,  abscess,  or  gangrene 
may  be  implanted  upon  the  vulnerable  bronchopneumonic  areas. 

Important  concomitant  pathologic  changes  of  catarrhal  pneumonia 
include  pleurisy  and  pleural  petechiae,  congestion  and  inflammation 
of  the  larger  bronchi,  and  edematous  swelling  of  the  peribronchial 
glands.  Empyema,  meningitis,  and  septic  arthritis  are  the  more 
common  complications,  which,  as  a  class,  are  rare,  while  exceptionally 
the  cardiac  muscle  and  the  endocardium  are  inflamed. 

As  a  rule,  catarrhal  pneumonia  arises  secondarily,  and  this  type 
of  the  disease  is  usually  of  streptococcal  origin;  primary  cases  ordi- 
narily are  either  pneumococcal  or  pneumostreptococcal.  The  dis- 


DISEASES   OF   THE    BRONCHOPULMONARY   SYSTEM          IQ5 

ease  is  most  common  in  the  extremes  of  life,  for  at  these  two  periods 
the  bronchovesicular  mucosa  is  unusually  susceptible  to  inflammatory 
processes  and  the  respiratory  musculature  too  enfeebled  to  insure 
thorough  expulsion  of  the  bronchiolar  secretions.  Catarrhal  pneu- 
monia is  a  grave  menace  to  life  in  many  of  the  acute  infections, 
notably  in  measles,  diphtheria,  pertussis,  scarlatina,  variola,  and 
enteric  fever,  and  it  is  also  prone  to  develop  in  subjects  of  nephritis, 
organic  cardiac  affections,  malignant  disease,  rickets,  emphysema, 
and  other  debilitating  and  resistance-lowering  conditions.  Tuber- 
culosis, syphilis,  anthrax,  and  other  specific  foci  in  the  lungs  are 
attended  by  catarrhal  inflammation  of  a  lobular  type,  and  the  same 
is  true  of  the  several  forms  of  pneumokoniosis.  Deglutition  or  aspir- 
ation pneumonia,  due  to  the  insufflation  of  minute  foreign  particles, 
is  met  with  in  various  comatose  states  (i.  e.,  uremia  and  apoplexy) 
in  which  the  sensitiveness  of  the  upper  respiratory  passages  is  abol- 
ished. Owing  to  this  defect,  fine  bits  of  contaminated  matter  (food- 
particles,  for  example)  may  be  sucked  into  the  bronchi,  whose  secretion 
carries  the  infection  downward  into  the  terminal  bronchial  twigs, 
and  thence  to  the  alveoli.  Aspiration  pneumonia  is  the  common  type 
of  pneumonitis  in  the  new-born,  and  it  also  develops  as  the  result 
of  infection  from  operations  about  the  mouth  and  upon  the  upper 
air-passages,  as  well  as  in  laryngeal  and  esophageal  cancer.  Ether 
pneumonia,  so  called,  is  generally  of  the  lobular  variety,  and  may 
prove  of  grave  consequence  in  an  otherwise  successful  operation. 
The  accident  doubtless  arises  from  a  number  of  causes— the  action 
of  the  ether  in  chilling,  irritating,  and  lowering  the  resistance  of  the 
bronchopulmonary  structures,  the  insufflation  of  infectious  matter 
from  a  contaminated  inhaler,  and  the  exposure  of  the  patient  while 
on  the  operating  table. 

Physical  Signs. — Inspection. — Inspection  is  of  the  utmost  clinical 
value,  for  fulminating  cases  sometimes  run  so  rapidly  fatal  a  course 
that  tactile  and  auditory  signs  fail  to  develop,  or  do  so  most  indefi- 
nitely. Dyspnea,  cyanosis,  and  distressing  cough  are  the  objective 
symptoms  to  which  attention  should  be  especially  directed.  The 
dyspnea,  with  corresponding  cyanosis,  is  noticeable  from  the  beginning 
of  the  attack,  and,  as  the  pulmonary  lesion  spreads,  becomes  progress- 
ively more  acute,  the  patient  gasping  for  breath  with  loud,  jerky, 
rapid  respiratory  efforts,  which  do  but  little  to  satisfy  the  call  for 
oxygen.  In  the  so-called  "suffocative  catarrh,"  ending  in  death 
from  asphyxia  and  cardiac  paralysis,  these  evidences  of  deficient 
aeration  are  most  strikingly  exhibited.  A  persistent  and  distressing 
"grunty"  cough,  usually  unproductive  and  often  painful,  begins 


196  PHYSICAL    DIAGNOSIS 

early  and  lasts  through  the  acute  stages,  though  in  fatal  cases  it  may 
abate,  despite  the  persistence  of  the  other  signs,  a  few  hours  before 
death.  The  patient's  flushed  cheeks  and  dry,  hot  skin  are  visible 
signals  of  the  existing  pyrexia.  In  the  event  of  extensive  basal  con- 
fluence of  the  lobular  consolidations,  inspiratory  drawing  in  of  the 
lower  ribs  and  interspaces  is  observed. 

Palpation. — Vocal  fremitus  is  exaggerated  if  the  lesions  be 
sufficiently  confluent  and  superficial  to  conduct  the  voice  vibrations 
to  the  surface  of  the  chest.  Widely  disseminated  and  deep  infiltra- 
tions, especially  if  separated  and  surrounded  by  emphysematous 
areas,  do  not  increase  tactile  fremitus,  but,  on  the  contrary,  may 
diminish  it. 

Percussion. — Early  in  the  attack  the  percussion  sound  is  unal- 
tered, and  in  fatal  cases  it  may  remain  so  until  the  end.  But  as  the 
infiltrations  grow  and  extend  toward  the  surface  of  the  lung, 
scattered  patches  of  impaired  resonance,  sometimes  amounting  to 
actual  dulness,  can  be  made  out.  Coexisting  emphysematous  ter- 
ritories, however,  may  ingraft  their  quality  upon  the  bronchopneu- 
monic  sound,  so  that  dull  hyperresonance  is  elicited.  Above  the 
site  of  consolidation,  where  there  is  vicarious  overdistention  of  the 
vesicles,  the  percussion  sound  is  likely  to  be  typically  hyperresonant. 

Auscultation. — The  respiration  is  either  bronchovesicular  or  purely 
bronchial,  according  to  the  conditions  holding  in  the  individual  case — 
bronchovesicular,  if  the  solid  patches  be  small  and  well  disseminated; 
bronchial,  if  they  crowd  one  another  or  are  confluent  throughout  a 
considerable  part  of  the  lobe.  The  seat  of  the  lesion,  whether  central 
or  peripheral,  and  the  condition  of  the  adjacent  vesicular  structure, 
whether  normal,  collapsed,  or  distended,  are  active  modifying  influ- 
ences of  the  respiratory  sounds.  Distinct  bronchophony,  perhaps 
pectoriloquy,  is  audible  over  the  consolidated  lobules,  the  determining 
factors  of  these  signs  being  substantially  the  same  as  those  affecting 
vocal  fremitus. 

Subcrepitant  rales  at  both  bases,  often  associated  with  dry  and 
piping  sibilant  sounds,  are  the  most  typical  auscultatory  findings  in 
catarrhal  pneumonia.  Finer  vesicular  crepitations  are  also  detected, 
so  long  as  the  lobular  solidification  is  not  complete,  and  in  many 
instances  there  are  the  numerous  dry  and  moist  rales  of  a  concomitant 
bronchitis  of  the  larger  tubes. 

Diagnosis. — The  gradual  development  of  fever,  rapid  and  labored 
breathing,  cough  and  viscid  expectoration,  with  subcrepitant  and 
crepitant  rales  scattered  over  both  bases,  is  highly  characteristic, 
despite  no  distinctive  modifications  of  the  respiratory,  vocal,  and 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM          197 

percussion  sounds.  Especially  significant  are  such  signs  when  they 
supervene  in  connection  with  one  of  the  acute  specific  infections, 
or  during  the  course  of  some  depressing  chronic  affection.  Distinctly 
impaired  resonance,  bronchial  breathing,  and  bronchophony,  though 
classic  signs,  can  be  detected  only  when  a  considerable  area  of  con- 
solidated tissue  lies  within  the  range  of  auscultation  and  percussion, 
and  in  the  average  case  of  catarrhal  pneumonia  the  diagnosis  must 
rest  upon  the  association  of  disseminated  fine  moist  rales  with  high 
fever  and  acute  respiratory  disturbances.  In  the  less  frequent  pri- 
mary form  of  the  infection,  however,  it  is  generally  possible  to  map 
out  circumscribed  areas  of  consolidation  which  are  peculiarly  prone 
rapidly  to  clear  up  and  to  reappear  in  other  regions. 

An  ambulant  form  of  confluent  bronchopneumonia  of  lobar  type 
in  young  adults  is  described  by  Riesman,  who  summarizes  its  chief 
clinical  features  as  cough,  moderate  fever,  and  a  protracted  course 
characterized  by  absence  of  initial  chill  and  critical  defervescence, 
ending  in  complete  recovery.  The  physical  signs  relate  to  an 
extensive  basal  lobar  consolidation— dulness,  bronchovesicular 
respiration,  and  abundant  showers  of  fine,  moist  crackling  rales, 
frequently  having  a  consonating  quality. 

From  croupous  pneumonia  the  secondary  type  of  catarrhal  pneu- 
monia can  be  distinguished  with  ease,  but  the  primary  type  only 
with  difficulty,  if  at  all.  In  the  secondary  form  the  gradual,  insidious 
onset  of  the  respiratory  stress,  the  early  bronchitic  symptoms,  the 
bilateral  distribution  of  the  chest  signs,  and  the  recovery,  by  lysis, 
stand  in  strong  contrast  to  the  abrupt  onset,  the  predominant  pleural 
symptoms,  the  unilateral  lobar  consolidation,  and  the  critical  ter- 
mination of  typical  croupous  pneumonia.  The  attempt  to  differ- 
entiate the  latter  from  catarrhal  pneumonia  of  the  primary  type 
must  needs  fail  in  those  instances  in  which  the  lobular  lesions  rapidly 
fuse  and  spread,  for  here  the  onset  is  abrupt,  the  fever  high,  the  sputum 
rusty,  and  the  physical  signs  those  of  dense  basal  consolidation.  In 
this  quandary  the  susceptibility  of  young  children,  especially  under 
the  age  of  one  year,  to  lobular  rather  than  to  lobar  inflammations,  the 
fleeting  tendency  of  a  lobular  pneumonia,  and  its  likelihood  of  becom- 
ing definitely  multiple  sooner  or  later,  are  to  be  remembered. 

Catarrhal  pneumonia  versus  bronchopneumonic  phthisis  is  an  impor- 
tant question  to  be  decided,  inasmuch  as  most  of  the  lobular  pneu- 
monias incident  to  measles  and  whooping-cough  are  of  tuberculous 
nature.  Unfortunately,  in  many  instances  the  differentiation  must 
be  postponed  until  the  tuberculous  inroads  become  unmistakable, 
or  until  the  subject  conies  to  autopsy.  A  tuberculous  history,  great 


IQ8  PHYSICAL    DIAGNOSIS 

prostration,  rapid  emaciation,  free  sweating,  recurrent  hemoptysis 
tubercle  bacilli  and  elastic  tissue  in  the  sputum,  and  softening, 
especially  apical,  are  the  principal  hall-marks  of  phthisical  cases. 

Acute  bronchitis  and  catarrhal  pneumonia  can  sometimes  be  dis- 
tinguished only  by  taking  into  account  the  relative  intensity  of  the 
fever,  cough,  dyspnea,  and  similar  disturbances  in  the  two  affections, 
for  in  both  the  physical  signs  may,  at  least  for  a  time,  be  practically 
identical.  (See  p.  173.) 

CROUPOUS    PNEUMONIA    (Fibrinous   or    Lobar   Pneumonia;    Pneu- 
monitis;   Lung  Fever) 

Clinical  Pathology. — Croupous  pneumonia  is  an  acute,  self- 
limited,  infectious  disease,  associated  with  a  constant  and  character- 
istic pulmonary  lesion  of  one  or  more  lobes  and  with  a  distinctive 
clinical  picture,  due  primarily  to  the  effects  of  the  specific  pneumo- 
toxin.  After  a  period  of  intense  congestion  the  pulmonary  structure 
becomes  consolidated  by  the  intra-alveolar  accumulation  of  a  coagul- 
able  fibrinous  exudate,  which  tends  subsequently  to  undergo  lique- 
faction and  removal  by  resorption  and  by  expectoration,  thus  resolv- 
ing the  consolidation  and  restoring  the  original  condition  of  the  affected 
lung.  Pneumonia  is  due  to  invasion  of  the  lungs  by  Fr^nkel's  pneu- 
mococcus,1  which  not  only  evolves  absorbable  toxins  in  the  local 
lesions,  but  itself  enters  the  general  circulation.  It  is  still  a 
moot  point  whether  the  infection  arises  by  the  inhalation  of 
dried  sputum  charged  with  pneumococci  or  by  auto-infection  from 
the  germs  commonly  resident  in  the  healthy  throat.  Other  bacteria 
with  which  the  pneumococcus  may  be  associated  include  Fried- 
lander's  pneumobacillus,  the  pyogenic  cocci,  and  the  bacilli  of 
enteric  fever,  diphtheria,  and  influenza.  These  microorganisms, 
however,  probably  have  no  direct  influence  in  exciting  true  croup- 
ous  pneumonia,  with  the  exception  of  the  first-named  bacterium, 
which  is  regarded  as  the  exciting  factor  of  a  grave  form  of  pneu- 
monitis  characterized  by  a  tendency  toward  necrosis  and  suppura- 
tion— "Friedlander  pneumonia." 

As  a  rule,  pneumonia  is  unilateral,  and  implicates  the  greater  part 
of  one  lobe,  particularly  the  lower  right  lobe;  less  commonly  an 
entire  lung  is  affected,  an  extensive  consolidation  -of  this  type  being 
somewhat  more  frequent  on  the  right  than  on  the  left  side.  The 
relative  incidence  of  the  commoner  sites  of  primary  pneumonic  le- 
sions is  illustrated  by  analysis  of  the  statistics  of  1500  cases  studied 

1  Discovered  by  Sternberg,  and  by  "him  named  Micrococcus  Pasteuri. 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        199 

by  Ashton  and  Landis,  by  Osier,  and  by  G.  W.  Norris,  which  shows 
that  the  right  lung  was  attacked  in  approximately  52  per  cent,  of  cases, 
the  left  lung  in  35  per  cent.,  both  lungs  in  14  per  cent.,  and  the  apex 
of  one  or  of  both  lungs  in  14  per  cent.  In  the  Philadelphia  General 
Hospital,  about  25  per  cent,  of  the  pneumonia  patients  have  consoli- 
dation of  the  right  lower  lobe,  22  per  cent,  of  the  left  lower  lobe,  12 
per  cent,  of  the  entire  lung,  and  less  than  2  per  cent  crossed  pneu- 
monia. 

The  situation  of  the  local  lesion  may  account  for  decided  contrasts 
in  the  clinical  features  of  different  cases  of  pneumonia,  and  in  con- 
sequence of  this,  numerous  special  forms  of  the  disease  have  been 
exploited  from  time  to  time,  usually  without  valid  reason.  Certain 
pathologic  variations,  however,  merit  separate  mention,  and  of  such 
the  following  seem  of  practical  importance.  Apex  pneumonia,  in 
which  the  initial  consolidation  invades  an  apex  of  the  lung,  generally 
on  the  right  side,  is  met  with  more  commonly  in  the  child  than  in 
the  adult,  is  frequently  provocative  of  grave  toxemia  attended  by 
striking  cerebral  symptoms,  tends  to  resolve  slowly,  and  always  suggests 
the  possibility  of  tuberculosis.  Double  pneumonia,  implicating  both 
lungs,  is  especially  prone  to  affect  the  lower  lobes,  while  crossed  pneu- 
monia, or  bilateral  lesions  of  an  opposite  base  and  apex,  more  often 
begins  in  the  right  upper  and  left  lower  than  in  the  left  upper  and  right 
lower  lobes.  Central  or  core  pneumonia  is  the  term  applied  to  a 
pneumonic  patch  deep  within  the  lung,  perhaps  so  remote  from  the 
surface  that  no  definite  physical  signs  are  afforded,  or,  when  present, 
are  not  recognizable  until  several  days  after  the  initial  chill.  Should 
the  pneumonitis  spread  in  the  form  of  a  vertical  slab  of  solidification, 
the  designation  stripe  pneumonia  is  applicable.  Superficial  pneu- 
monia is  so  named  because  in  this  variety  the  process  primarily 
affects  the  surface  of  the  lung  directly  beneath  the  pleura,  and  hence 
the  physical  signs  of  the  pneumonic  lesion  are  peculiarly  easy  of 
detection  and  the  evidences  of  the  concurrent  pleurisy  conspicuous. 
(See  Pleuropneumonia,  p.  203.)  Wandering  pneumonia  is  a  form 
of  the  infection  that  slowly  and  persistently  creeps  through  the  lungs, 
successively  attacking  lobe  after  lobe,  either  by  direct  continuity 
(pneumonia  errans),  or  by  the  establishment  of  independent  foci 
(pneumonia  migrans)  remote  from  the  original  lesion;  a  lung  thus 
implicated  may  show  simultaneously  all  stages  of  the  pneumonic 
process,  and  the  symptoms  therefrom  are  likely  to  be  protracted, 
disorderly,  and  grave.  The  adjective  massive  is  applied  to  that 
form  of  pneumonia  in  which  not  only  the  alveoli,  but  also  the  bronchi, 
of  a  lobe,  or  even  of  an  entire  lung,  are  choked  with  a  fibrinous  exu- 


200  PHYSICAL   DIAGNOSIS 

date,  and  in  this  rare  condition  the  auscultatory  physical  signs  are 
effectually  negatived  by  the  extensive  bronchial  obstruction.  The 
physical  signs  of  a  massive  pneumonia  are  very  similar  to  those  of 
pleural  effusion. 

During  its  evolution  the  pneumonic  lesion  passes  through  three  prin- 
cipal stages:  congestion,  red  hepatization,  and  gray  hepatization, 
with  which  it  is  possible  to  correlate  more  or  less  distinctive  physical 
signs.  Pathologically,  these  three  stages  are  not  always  sharply 
defined,  for  a  lung  attacked  by  a  rapidly  spreading  pneumonic  inflam- 
mation may  be  the  seat  of  every  possible  phase  of  the  process  simultan- 
eously. 

The  stage  of  congestion  or  engorgement,  usually  lasting  less  than 
twenty-four  hours,  begins  as  an  intense  inflammatory  engorgement 
of  the  interalveolar  capillaries  with  the  subsequent  leakage  of  serum 
hence  into  the  adjacent  air-cells.  The  latter,  when  this  stage  is 
fully  developed,  are  partly  filled  with  a  serous  exudate  containing  a 
few  leukocytes  and  erythrocytes,  together  with  swollen,  granular 
epithelial  cells  shed  from  the  alveolar  wall.  Macroscopically,  the 
lung  appears  enlarged,  dark  red  in  color,  and  abnormally  moist; 
although  denser  than  normal  and  of  diminished  resiliency,  the  pul- 
monary tissue  still  crepitates,  and  contains  sufficient  air  to  keep  it 
afloat  when  placed  in  water. 

In  the  stage  of  red  hepatization  or  dense  consolidation,  of  about 
four  or  five  days'  duration,  the  initial  capillary  engorgement  still 
persists,  the  interalveolar  walls  are  infiltrated  and  edematous,  and 
the  alveoli,  hitherto  the  seat  of  but  a  moderate  exudate,  are  now 
completely  filled  with  a  highly  coagulable  serofibrinous  exudate, 
rich  in  fibrin  and  full  of  erythrocytes,  leukocytes,  bacteria,  and 
desquamated  epithelium  (Fig.  97).  On  section,  the  lung  appears 
unduly  dry,  although  when  scraped  with  a  knife  a  small  amount  of 
sanguineous  fluid  mixed  with  minute  fibrinous  masses  exudes  along 
the  track  of  the  blade;  the  cut  surface  is  stippled  with  numerous 
granular  areas  corresponding  to  the  alveolar  and  bronchiolar  coagula 
of  fibrin.  The  area  thus  consolidated  and  enlarged  is  of  a  deep-red 
or  brownish-red  color,  resembling  a  piece  of  liver — hence  the  appro 
priate  term,  red  hepatization;  the  tissue  of  the  lung  tears  easily,  and  is 
so  dense  and  so  airless  that  it  neither  crepitates  nor  floats. 

As  gray  hepatization  and  resolution  supervene,  the  consolidation 
becomes  gray  or  grayish-yellow  in  appearance,  being  either  of  a  fairly 
uniform  tint  or  mottled  with  patches  of  persistent  red  hepatization 
(Fig.  98) .  The  lung  is  smaller,  moister,  and  less  granular  than  in  the 
immediately  preceding  stage,  and,  as  resolution  advances,  the  vesic- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        2OI 

ular  tissue  becomes  correspondingly  crepitant;  elastic,  and  less 
friable.  These  gross  changes  indicate  subsidence  of  the  primary 
capillary  engorgement,  active  leukocytic  infiltration  of  the  inter- 
alveolar  walls,  and  gradual  shrinkage,  softening,  and  liquefaction 
of  the  exudate.  The  character  of  the  latter  is  now  altered  by  the 
disappearance  of  the  erythrocytes  and  of  the  dense  fibrin  network, 


Fig.  97. — Croupous  pneumonia;  stage  of  red  hepatization  (Jefferson  Hospital  Labora- 
tories). 

and  by  the  influx  of  many  leukocytes  which,  so  to  speak,  clean  up 
much  of  the  bacterial  and  cellular  detritus  of  the  vesicles  by  phago- 
cytosis. The  exudate,  having  undergone  fatty  degeneration  and 
dissolution,  is  finally  disposed  of  by  the  lymphatics  and  by  expectora- 
tion, complete  resolution  of  the  pneumonic  area  and  adequate  aera- 
tion of  the  lung  being  effected  within  a  fortnight  or  sooner,  in  favor- 


2O2 


PHYSICAL   DIAGNOSIS 


able  cases.  Occasionally  gray  hepatization  is  succeeded  by  a  stage  of 
pundent  infiltration,  in  consequence  of  which  the  consolidated  parts 
take  on  a  yellowish  color  from  their  permeation  by  an  abundant 
purulent  exudate,  and  become  soft,  boggy,  and  exceedingly  friable. 
Pus-cells  flood  the  alveoli  and  extensively  infiltrate  the  pulmonary 
connective  tissue,  as  the  result  of  which  the  lung  ultimately  may  be 


Fig.  98. — Croupous  pneumonia;  stage  of  gray  hepatization  (Jefferson  Hospital  Labora- 
tories). 

riddled  with  abscesses  of  various  size,  should  the  process  persist 
unresolved. 

Delayed  resolution  of  the  consolidation  is  said  to  exist  when,  despite 
the  subsidence  of  the  active  pneumonic  symptoms,  the  physical  signs 
indicate  the  persistence  of  an  exudate  undergoing  slow,  imperfect 
liquefaction  and  removal  from  the  alveoli.  In  simple  delayed  resolu- 
tion weeks  may  pass  before  the  consolidation  entirely  disappears 
and  the  function  of  the  lung  is  restored.  On  the  other  hand,  the 
lung  may  never  clear  up,  but,  by  fault  of  a  fibroid  overgrowth  starting 


DISEASES    OF    THE   BRONCHOPULMONARY    SYSTEM        203 

in  the  interalveolar  structures,  become  the  seat  of  a  dense  cirrhosis 
which  obliterates  the  air-cells  and  greatly  contracts  the  pulmonary 
parenchyma.  In  other  cases  pulmonary  abscess  is  the  sequel  of  a 
delayed  resolution,  and,  rarely,  gangrene  develops.  Tuberculosis 
may  follow  pneumonia,  should  the  latter  light  up  a  quiescent  tuber- 
culous lesion.  "The  instances  of  caseous  pneumonia  and  softening 
which  have  followed  an  acute  pneumonic  process  have  been  from  the 
outset  tuberculous"  (Osier). 

Fibrinous  pleurisy  is  a  practically  constant  accompaniment  of  pneu- 
monia, save  in  deep-seated  central  lesions  that  resolve  without  reach- 
ing the  surface  of  the  lung.  Usually  the  inflammation  attacks  the 
pleura  contiguous  to  the  pneumonic  area,  but  it  may  also  rapidly 
extend  over  the  non-pneumonic  lobes.  Indeed,  pleurisy  may  be 
so  dominant  a  feature  as  to  justify  the  use  of  the  old  term  "pleuro- 
pneumonia."  Ordinarily,  the  pleurisy  clears  up  as  the  pneumonia 
undergoes  resolution,  but  it  may  result  in  permanent  adhesion  and 
thickening  of  the  pleural  surfaces,  in  a  richly  fibrinous  effusion  so 
large  as  to  require  aspiration,  or  in  an  empyema  removable  only 
by  free  incision.  Catarrhal  bronchitis  commonly  is  associated  with 
pneumonia,  and  in  many  cases  there  is  inflammatory  enlargement  of 
the  bronchial  glands.  The  larger  bronchial  tubes  contain  an  abun- 
dant serous  fluid  with  a  variable  amount  of  fibrinous  material,  and 
the  smaller  tubes  traversing  the  pneumonic  area  may  be  choked  with 
tough  plugs  of  fibrin.  Inflammation  of  the  endocardium  and  peri- 
cardium are  important  and  not  very  infrequent  complications  of 
pneumonia.  Endocarditis  is  the  commoner  of  the  two,  and  more  espe- 
cially implicates  the  valves  of  the  left  than  of  the  right  heart,  particu- 
larly attacking  those  leaflets  whose  vulnerability  has  been  heightened 
by  chronic  valvulitis.  The  pneumococcus  infection  may  be  quiescent 
and  inconspicuous,  or  it  may  light  up  a  .most  virulent  malignant 
endocarditis,  with  striking  toxemia,  symptoms  of  septic  embolism, 
and  signs  of  valve  destruction.  Pericarditis  is  particularly  prone 
to  occur  in  infantile  pneumonia,  especially  of  the  left  lung.  It  may 
follow  a  relatively  benign  course,  or  it  may  result  in  the  collection  of 
a  serofibrinous  or  purulent  effusion  of  sufficient  volume  to  produce 
unmistakable  physical  signs.  Actual  myocarditis,  sufficiently  ad- 
vanced to  attract  attention,  rarely  occurs,  save  as  the  result  of  pro- 
longed, intense  attacks,  but  the  heart  muscle  not  infrequently 
shows  cloudy  swelling,  or,  rarely,  more  advanced  degeneration. 
Arthritis  is  sometimes  seen  in  association  with  pneumonia,  especially 
in  the  young;  the  joint  swelling  may  precede  the  pneumonia,  appear 
during  its  height,  or  develop  after  defervescence.  Other  complica- 


204  PHYSICAL    DIAGNOSIS 

tions  of  pneumonia  of  infrequent  incidence  include  meningitis, 
neuritis,  peritonitis,  croupous  gastritis  and  colitis,  acute  gastric 
dilatation,  venous  thrombosis,  otitis  media,  and  parotid  bubo. 

Physical  Signs. — Inspection. — The  pneumonic  facies  is  charac- 
terized by  an  anxious,  alert  expression,  by  flushed  cheeks  and  shining 
eyes,  by  crops  of  herpes  about  the  lips  and  nose,  and  by  inspiratory 
gaping  of  the  nostrils.  Cyanosis  is  sometimes  observed,  but,  as  a 
rule,  it  is  not  conspicuous;  and  in  the  bilious  type  of  the  disease 
jaundice  develops,  often  most  intensely.  The  patient  generally 
lies  upon  the  affected  side,  and  breathes  rapidly,  laboriously,  and 
painfully,  owing  to  the  action  of  the  pneumotoxin,  to  restriction  of 
the  aerating  surface  of  the  lungs,  and  to  pleural  pain.  Very  commonly 
respiration  is  punctuated  by  a  peculiar  and  quite  distinctive  "expira- 
tory grunt."  The  dyspnea,  though  urgent,  rarely  amounts  to  actual 
orthopnea.  The  respiratory  rate  may  be  two,  three,  or  even  four  times 
more  rapid  than  normal.  The  typical  pneumonic  cough  is  frequent, 
dry,  and  painful,  hence  repressed.  The  chest  movements  are  limited 
on  the  affected  side,  especially  in  extensive  consolidations  and  in 
those  accompanied  by  wide-spread  pleurisy.  On  the  unaffected 
side  there  are  vicariously  exaggerated  respiratory  movements,  and 
the  same  thing  is  to  be  noted  over  the  upper  lobe  of  a  lung  extensively 
consolidated  at  its  base.  This  condition  also  may  mechanically 
restrict  the  diaphragm  excursions  on  the  side  of  the  lesion,  but  in 
other  instances  pleural  or  diaphragmatic  inflammation  accounts  for 
an  absence  of  the  normal  diaphragm  shadow.  The  cardiac  impulse 
may  be  transmitted  with  undue  force  by  dense  consolidation  of  the 
thin  wedge  of  the  left  lung  which  extends  downward  in  front  of  the 
pericardium. 

The  sputum  at  first  is  generally  mucoid,  but  as  hepatization  sets 
in,  exceedingly  viscid,  tenacious  matter,  often  streaked  with  bright 
red  blood,  is  expectorated,  generally  with  great  difficulty;  later  the 
sputum  tends  to  become  of  red-brown  hue,  or  "rusty."  The  sputum 
may  be  tinged  yellow  or  green  when  jaundice  coexists,  and  is  thin  and 
dark  colored,  like  prune-juice,  in  asthenic  subjects;  it  is  abundantly 
mucopurulent  when  there  is  severe  attendant  bronchitis,  and  conspicu- 
ously hemorrhagic  in  severe  sthenic  cases;  in  the  aged,  in  the  very 
young,  and  in  the  debilitated  little  or  nothing  may  be  expectorated. 
After  crisis  copious  puriform  sputum  is  the  rule,  none  at  all,  the  ex- 
ception. Microscopically,  pneumonic  sputum  consists  chiefly  of  ery- 
throcytes,  leukocytes,  alveolar  and  bronchial  epithelium,  small 
bronchiolar  casts  of  fibrin,  and  pneumococci,  ordinarily  mixed  with 
other  microorganisms. 


DISEASES    OF    THE    BRONCHOPULMONA*RY    SYSTEM        205 

By  x-ray  examination  with  a  fluoroscope  the  detection  of  a  shadow 
toward  the  center  or  lower  part  of  the  lung  is  most  suggestive,  par- 
ticularly if,  on  subsequent  examinations,  such  a  shadow  be  found  to 
change  in  accordance  with  the  extension  and  resolution  of  a  pneu- 
monic area.  Especially  in  central  pneumonias  is  the  x-ray  able  to 
reveal  consolidated  patches  too  deep  to  give  convincing  percussion 
signs.  In  most  instances  the  fluoroscope  also  indicates  a  restricted 
diaphragm  excursion  on  the  pneumonic  side,  and  in  some  it  shows 
cardiac  displacement  and  even  right-sided  enlargement. 

Palpation. — The  rapid,  restricted  respiratory  movements  and  the 
anevenness  of  expansion  noted  on  inspection  are  clearly  recognized 
by  the  palpating  palm,  by  which  pleural  friction  is  also  occasionally 
appreciated.  As  the  vesicles  fill  with  the  exudate,  vocal  fremitus 
increases,  reaching  its  acme  with  complete  hepatization  and  becoming 
normal  again  with  the  resorption  of  the  exudate.  It  is  important 
to  remember  that  vocal  fremitus  may  be  entirely  cut  off  by  a  coexist- 
ing pleural  effusion  or  by  the  obstruction  of  a  bronchus  leading  from 
the  pneumonic  patch. 

The  pulse,  full  and  bounding  at  the  beginning  of  the  attack,  tends 
progressively  to  diminish  in  volume  and  in  force  as  the  infection 
progresses.  The  rate  of  the  pulse  ordinarily  corresponds  to  the 
degree  of  pyrexia,  but  the  usual  pulse-respiration  ratio  is  greatly 
disturbed,  commonly  ranging  from  2  or  3  to  i,  and,  in  exceptional 
cases,  being  practically  equal.  A  pulse-rate  exceeding  120  is  a  grave 
omen,  save  in  children  in  whom  a  much  greater  frequency  does  not 
necessarily  imperil  life.  From  150  to  170  is  the  usual  pulse-rate 
in  young  children  and  infants  affected  with  lolmr  pneumonia. 

Excessive  rapidity  of  the  pulse,  irregularities  of  volume,  and 
arhythmia  are  danger  signals,  especially  "when  they  appear  before 
crisis. 

The  blood-pressure  in  the  average  case  of  pneumonia  shows  no 
noteworthy  changes,  but  a  striking  hypotension  is  an  unfavor- 
able sign.  Gibson's  rule  is  but  approximate:  "When  the  systolic 
pressure  in  millimeters  does  not  fall  below  the  pulse-rate  in  beats 
per  minute,  the  fact  is  of  good  augury;  when  the  pulse-rate  per 
minute  is  higher  than  the  millimeters  of  blood-pressure,  the  equi- 
librium of  the  circulation  is  seriously  disturbed." 

Percussion. — During  the  stage  of  engorgement  exaggerated  reso- 
nance, commonly  of  a  Skodaic  quality,  is  found  over  the  affected  lung, 
and  a  similar  hyperresonance  is  also  elicited  above  the  level  of  a 
hepatized  area.  In  pneumonia  of  an  upper  lobe  Wintrich's  sign 
(heightened  pitch  and  increased  intensity  of  the  hyperresonance  when 


206  PHYSICAL    DIAGNOSIS 

the  patient's  mouth  is  open)  is  frequently  demonstrable,  and  a  cracked- 
pot  percussion  sound  is  not  uncommon.  As  the  hepatization  pro- 
gresses the  dulness  becomes  correspondingly  pronounced  and  the 
resistance  to  pleximeter  finger  appreciably  increases,  but  as  resolution 
occurs  these  signs  gradually  disappear  and  sooner  or  later  are  replaced 
by  normal  pulmonary  resonance — soon  in  the  average  case;  late  in 
the  exceptional  one,  in  which,  despite  a  typical  crisis  and  no  unfavor- 
able symptoms,  the  days  may  lengthen  into  weeks  before  the  defec- 
tive resonance  wholly  disappears.  Over  a  central  pneumonia  dulness 
develops  both  slowly  and  imperfectly,  and,  should  such  an  infiltration 
resolve  without  invading  the  periphery  of  the  lung,  nothing  more 
definite  than  a  moderate  impairment  of  resonance  may  be  detected. 
In  extensive  unilateral  consolidations  the  opposite  lung  is  vicariously 
hyperresonant.  The  area  of  cardiac  flatness  may  extend  unduly 
beyond  the  right  border  of  the  sternum,  and  frequently  the  percus- 
sion limits  of  the  liver  and  the  spleen  are  enlarged. 

Auscultation. — Early  during  the  stage  of  engorgement  the  respira- 
tory murmur  ordinarily  is  feeble  and  suppressed,  but  as  the  infiltra- 
tion progresses  the  sound  becomes  harsher  and  more  exaggerated, 
until  the  vesicular  element  is  replaced  first  by  bronchovesicular 
breathing,  and  later,  when  there  is  well-defined  hepatization,  by 
loud  and  tubular  bronchial  breathing.  The  latter's  great  intensity, 
high  pitch,  and  distinctive  "hu-u-u"  quality  are  most  conspicuous 
over  a  consolidation  adjacent  to  a  large,  perfectly  patent  bronchial 
tube,  and  sometimes  the  amplication  of  the  bronchial  tone  is  so  great 
that  it  is  audible  some  distance  away  from  the  pneumonic  focus. 
Usually  bronchial  breathing  cannot  be  detected  over  a  deep- 
seated  central  consolidation,  nor  is  it  audible  if  the  bronchi  be 
occluded,  as  by  a  fibrinous  plug  or  by  the  generalized  obstruction  of 
a  massive  pneumonia.  As  resolution  proceeds,  the  respiratory  sounds 
lose  their  bronchial  character,  become  bronchovesicular  again,  and 
finally  acquire  the  breezy  vesicular  quality.  The  intensity  of  the 
voice  resonance  corresponds  to  that  of  the  vocal  fremitus,  bron- 
chophony,  and  perhaps  whispering  pectoriloquy  being  heard  over  a 
consolidated  area,  and,  less  commonly,  even  egophony. 

Crepitant  rales,  in  volleys  'or  showers,  are  audible  at  the  end  of 
inspiration  during  the  stages  of  engorgement  and  of  resolution,  the 
crepitus  redux  of  the  latter  period  being  at  first  mingled  with, 
and  then  replaced  by,  larger  moist  rales  due  to  the  outpouring 
of  secretion  into  the  smaller  bronchi.  Pneumonia  in  an  emphyse- 
matous  subject  may  afford  no  crepitant  rales  whatever,  because  the 
alveoli  are  so  dilated  and  their  walls  so  rigid  that  there  can  be  no 


DISEASES    OF   THE    BRONCHOPULMONARY   SYSTEM        207 

mural  adhesion  and  separation  during  expiration  and  inspira- 
tion respectively.  In  young  children  crepitations  are  sometimes 
difficult  to  appreciate,  owing  to  inadequate  inspiratory  excursions  of 
the  thorax.  Since  the  vesicles  and  infundibula  are  distended  by  a 
fibrinous  exudate  during  the  stage  of  red  hepatization,  crepitant  rales 
are  then  inaudible,  save  perhaps  for  an  occasional  isolated  crackle 
produced  in  a  vesicle  which  has  escaped  complete  filling.  Pleural 
friction-sounds,  however,  are  not  infrequently  heard  at  this  time, 
as  well  as  during  the  other  stages  of  the  disease.  Moist  and  dry 
rales,  indicating  concurrent  local  or  general  bronchitis,  are  often  a 
prominent  associated  sign,  and  such  sounds  have  an  extraordinarily 
sharp,  resonant  quality  (consonating  rales)  when  they  arise  within 
bronchi  invested  by  compactly  consolidated  lung. 

The  cardiac  sounds,  at  first  intense  and  clear,  become  distant  and 
impure  during  the  height  of  the  fever,  and  relative  murmurs  denoting 
dilatation  of  the  mitral  and  tricuspid  orifices  sometimes  develop. 
So  long  as  the  right  ventricle  reacts  adequately  to  the  stress  imposed 
by  the  intrapulmonary  hypertension,  the  pulmonic  second  sound  is 
accentuated  and  of  unduly  high  pitch.  Gradual  weakening  of  the 
pulmonic  second  sound  is  an  important  sign  of  right  ventricular 
dilatation  consequent  to  the  pulmonary  engorgement,  actual  enfeeble- 
ment  of  the  valvular  tone  being  foreshadowed  by  a  lowering  of  its 
vicariously  heightened  pitch,  to  which  change  J.  M.  Anders  ascribes 
great  value  as  the  earliest  indication  of  right  heart  failure.  Irregu- 
larities of  rate,  rhythm,  and  force  appear,  as  the  strength  of  the 
heart  flags  under  the  influence  of  the  fever  and  the  pneumotoxhi. 
Sudden  death  may  occur,  without  warning,  from  acute  dilatation 
or  from  pulmonary  thrombosis.  Recent  studies  by  Porter  con- 
tradict the  former  view  that  the  circulatory  failure  in  pneumonia 
is  largely  ascribable  to  vasomotor  paresis. 

Diagnosis. — Frank  croupous  pneumonia  is  easily  recognized,  for 
in  no  other  disease  is  there  a  more  distinctive  clinical  picture,  of 
which  the  facies,  the  painful  cough  and  dyspnea,  the  rusty  sputum, 
the  abnormal  pulse-respiration  ratio,  and  the  orderly  development  of 
physical  signs  of  lobar  engorgement,  consolidation,  and  resolution 
are  the  noteworthy  features.  As  a  rule,  these  signs  follow  a  severe 
initial  chill,  and  are  accompanied  by  high  fever  reaching  its  acme 
within  a  few  hours  and  continuing  high,  with  trifling  fluctuations, 
for  from  about  five  to  ten  days,  when  it  abruptly  drops,  by  crisis. 
During  this  febrile  period  such  laboratory  findings  as  hyperinosis, 
leukocytosis,  iodophilia,  pneumococcemia,  and  striking  deficiency 
of  the  urinary  chlorids  constitute  important  corroborative  evidence. 


208  PHYSICAL    DIAGNOSIS 

After  crisis  the  urgent  symptoms  of  the  infection  rapidly  abate, 
the  normal  pulse-respiration  ratio  is  reestablished,  the  signs  of  con- 
solidation clear  up,  and  the  abnormal  blood  and  urine  changes 
disappear. 

Atypical  pneumonia,  however,  is  not  so  well  denned,  and  the  symp- 
tomatology outlined  above  is  subject  to  extraordinary  modifications 
according  to  the  ruling  factors  at  work  in  the  individual  case,  of  which 
influences  the  most  important  relate  to  the  virulence  of  the  invading 
bacteria,  the  age,  habits,  and  resistance  of  the  patient,  and  the  presence 
or  absence  of  coexisting  disease.  Such  factors  as  these  must  auto- 
matically recur  to  one  who  would  deal  successfully  with  the  diagnosis 
of  a  disease  capable  of  appearing  in  the  many  different  guises  which 
pneumonia  may  assume.  From  a  clinical  viewpoint,  the  following 
aberrant  types  of  pneumonia  are  of  sufficient  importance  to  call  for 
special  consideration. 

Larval  Pneumonia. — This  is  a  mild,  abortive,  ephemeral  type  of 
the  disease,  with  trifling  symptoms  and  poorly  defined  physical  signs, 
lasting  but  a  few  days  and  terminating  usually  by  a  most  rapid  crisis. 
In  this  class  belongs  the  one-day  pneumonia,  which  clears  up  by 
the  second  day  after  the  onset  of  the  initial  symptoms.  Many  cases 
of  so-called  epidemic  pneumonia,  extensively  prevailing  in  institutions, 
also  conform  to  this  type,  though  by  no  means  is  this  invariably  true, 
inasmuch  as  in  certain  epidemics  of  this  sort  the  symptoms  are  severe, 
particularly  those  relating  to  the  nervous  and  the  gastro-intestinal 
systems.  Epidemic  pneumonia  is  frequently  characterized  by  slow 
infiltration,  by  the  rapid  supervention  of  gray  hepatization,  and  by  a 
tendency  toward  connective-tissue  overgrowth  in  the  lungs. 

Toxic  Pneumonia. — In  contrast  to  the  above  there  is  a  toxic  or 
typhoid  pneumonia,  which  is  distinguished  by  grave  toxic  symptoms 
referable  to  a  bacteremia,  either  pneumococcic  or  mixed.  Early 
and  striking  prostration,  serious  cardiac  failure,  excessive  diarrhea, 
tympanites,  stubborn  headache,  delirium,  and  conspicuous  nervous 
symptoms  serve  in  such  instances  to  divert  attention  from  the  real 
cause  of  the  toxemia,  which  masquerades  as  enteric  fever  with  severe 
initial  pulmonary  lesions.  This  typhoid  pneumonia,  which  is  merely 
pneumonia  plus  the  "typhoid  state,"  is  to  be  distinguished  from 
pneumotyphus,  or  enteric  fever  complicated  at  the  outset  by  a  croup- 
ous  pneumonia  which  dominates  the  clinical  picture  for  the  first  week 
or  two.  In  typhoid  pneumonia  such  evidences  as  early  pneumococ- 
cemia,  persistently  negative  Widal  tests,  deficient  urinary  chlorids, 
and  absence  of  a  roseola,  together  with  the  critical  disappearance 
of  both  signs  and  symptoms,  serve  to  rule  out  a  concurrent  Eberth 


DISEASES    OF    THE   BRONCHOPULMONARY    SYSTEM        2OQ 

infection  and  to  stamp  the  condition  true  pneumonitis  with  grave 
toxic  manifestations.  In  pneumotyphus,  on  the  other  hand,  the 
expected  crisis  fails  to  occur,  as  it  should  do  in  uncomplicated  pneu- 
monia within  a  fortnight,  and  by  the  end  of  this  period,  at  the  very 
latest,  the  distinctive  evidences  of  enteric  fever,  hitherto  overshadowed 
by  the  pneumonia,  begin  to  appear,  as  the  pulmonary  consolidation 
undergoes  resolution  and  the  enteric  lesions  approach  maturity. 

Aside  from  these  two  forms  of  true  toxic  pneumonia,  dulness  at 
the  right  base  posteriorly,  due  solely  to  an  intense  hepatic  conges- 
tion and  in  no  way  related  to  a  pulmonary  consolidation,  has  been 
described  by  Lesieur  and  Marchand  as  a  frequent  finding  at  the 
height  of  the  disease  in  uncomplicated  enteric  fever. 

Certain  cases  merit  the  term  bilious  pneumonia,  owing  to  the 
prominence  of  jaundice,  yellowish  or  greenish  sputum,  hepatic 
engorgement,  and  obstinate  vomiting;  some  of  these  are  possibly 
true  examples  of  toxemic  jaundice,  and  run  a  severe,  often  fatal, 
course,  while  others  are  simply  pneumonia  with  an  associated  ob- 
structive jaundice,  the  coexistence  of  which  does  not  materially 
affect  the  subject's  chances  of  recovery. 

Infantile  Pneumonia. — True  croupous  pneumonia  in  infants  and 
young  children,  though  commonly  attended  by  alarming  nervous  symp- 
toms, is  of  surprisingly  low  mortality.  Convulsions  and  vomiting  may 
replace  the  initial  chill,  and  delirium,  hyperpyrexia,  abdominal  pain, 
and  diarrhea  are  conspicuous  symptoms.  In  children  old  enough  to  ex- 
pectorate, the  sputum  is  more  likely  to  be  scanty  and  mucoid,  than 
profuse  and  rusty,  in  character.  In  about  one-half  of  all  cases  of 
infantile  pneumonia  the  patellar  reflex  is  abolished  during  the  stage 
of  acute  pyrexia;  frequently  the  knee-jerk  is  lost  before  the  develop- 
ment of  the  chest  signs,  and  ordinarily  it  returns  with  crisis  or 
shortly  afterward.  Apical  pneumonia  is  much  more  common  in 
children  than  in  adults,  the  spread  of  the  consolidation  and  its  subse- 
quent resolution  are  less  rapid,  and  the  occurrence  of  pericarditis 
and  of  acute  arthritis  is  more  frequent. 

Senile  Pneumonia. — Pneumonia  in  the  elderly  subject  has  an 
extremely  high  death-rate,  and  commonly  begins  without  an  initial 
chill,  the  onset  being  gradual  and  ill  defined.  The  leading  features 
of  the  attack  consist  of  great  prostration,  cardiac  asthenia,  moderate 
fever,  little  or  no  chest  pain,  and  slight  cough,  productive  of  scanty 
sputum,  perhaps  of  a  "prune-juice"  appearance.  Usually  the 
physical  signs,  which  are  prone  to  be  of  a  fleeting,  wandering 
character,  are  not  well  marked,  and,  indeed,  they  are  sometimes  quite 
effectually  masked  by  a  preexisting  emphysema;  resolution,  when  it 
14 


210  PHYSICAL   DIAGNOSIS 

does  occur,  is  prone  to  progress  slowly  and  imperfectly,  and  not 
infrequently  terminates  in  abscess  or  in  gangrene. 

Alcoholic  Pneumonia. — In  the  pneumonia  of  alcoholic  sub- 
jects the  symptomatology  suggests  delirium  tremens  rather  than 
to  pulmonary  consolidation,  for  the  clinical  picture  is  made  up 
of.  insomnia,  incoherent  muttering,  and  terrifying  hallucinations, 
which  develop  insidiously,  with  little  or  no  cough,  fever,  or  chest 
pain.  The  expectoration  is  frequently  like  prune-juice,  and  may 
be  quite  copious.  The  physical  signs,  however,  are  usually  char- 
acteristic, so  that  one  cannot  be  excused  for  overlooking  a  pneumonic 
lung  simply  because  the  patient  happens  to  be  raving  in  mania  a  potu. 
In  the  majority  of  alcoholics  pneumonia  is  equivalent  to  a  death- 
warrant. 

Traumatic  Pneumonia. — This  term  is  used  to  designate  a  form  of 
pneumonia  secondary  to  violent  injury  of  some  part  of  the  body  near 
or  remote  from  the  lungs,  or  arising  in  consequence  of  direct  laceration 
of  the  pulmonary  tissue.  The  affection  may  occur  indirectly,  from 
lowered  vital  resistance  produced  by  the  injury,  and  in  such  instances 
the  pulmonary  lesion  may  not  supervene  until  the  subject  has  been 
bed-ridden  for  some  weeks;  or  the  pneumonia  may  be  the  direct 
consequence  of  a  damaged  lung,  in  which  event  it  develops  within  a 
few  days  after  the  accident.  Contusion  pneumonia  is  a  variety 
of  pneumonitis  excited  by  a  violent  blow  upon  the  chest-wall. 

Intercurrent  and  Terminal  Pneumonia. — In  various  acute  specific 
infections,  notably  diphtheria,  influenza,  tuberculosis,  enteric  fever, 
typhus  fever,  bubonic  plague,  and  malarial  fever,  pneumonia  develops 
as  a  secondary,  sometimes  as  a  terminal,  process.  As  the  latter, 
it  is  also  met  with  in  certain  chronic  diseases,  of  which  diabetes, 
arteriosclerosis,  and  chronic  lesions  of  the  heart  and  kidneys  are 
typical  examples.  Intercurrent  and  terminal  pneumonias  are  not 
uncommonly  masked  by  the  symptoms  of  the  primary  disease,  and 
tend  to  pursue  a  more  or  less  latent  course,  lacking  the  dramatic  inva- 
sion, the  characteristic  febrile  stage,  and  the  clear-cut  physical  signs 
of  a  frank  primary  pneumonitis;  indeed,  in  many  instances  the  exist- 
ence of  pneumonia  is  determined  only  after  repeated  and  systematic 
physical  examinations,  and,  sometimes,  not  until  autopsy.  In  view 
of  these  facts  one  must,  aside  from  the  laboratory  side-lights,  often 
base  the  diagnosis  upon  somewhat  equivocal  evidence — moderate 
fever,  slight  increase  in  the  pulse  and  respiration  rates,  and  trifling 
cough,  with  impaired  resonance,  feeble  respiration,  and  a  few  crepita- 
tions at  the  base  of  a  lung. 

Aspiration  and  ether  pneumonias,  being  nearly  always  of  the  lobular 
type,  are  dealt  with  under  catarrhal  pneumonia.  (See  p.  192.) 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        211 

Aside  from  the  preceding  atypical  varieties  of  croupous  pneumonia 
there  remain  for  diagnostic  consideration  a  group  of  thoracic  diseases 
and  certain  acute  infectious  processes  which,  to  a  greater  or  less 
degree,  resemble  the  subjective  and  objective  symptoms  of  lobar 
consolidation.  The  first  group  comprises  pulmonary  congestion, 
edema,  infarction,  phthisis,  catarrhal  pneumonia,  pleural  effusion, 
and  bronchitis;  and  to  the  second  belong  meningitis  and  peri- 
tonitis. 

Acute  pulmonary  congestion,  in  so  far  as  the  clinical  picture  is  con- 
cerned, is  to  all  intents  and  purposes  the  initial  stage  of  croupous 
pneumonia;  it  is  distinguished  from  the  latter  by  its  short  duration, 
by  the  absence  of  lobar  consolidation,  and  by  the  non-development,  in 
orderly  succession,  of  the  attendant  pneumonic  phenomena.  In 
this  connection  "one-day  pneumonia"  and  Woillez's  "idiopathic  con- 
gestion" (q.  v.}  are  to  be  recalled. 

Hypostatic  congestion  usually  causes  dulness,  harsh  respiratory 
sounds,  exaggerated  fremitus,  and  crepitant  rales  at  the  bases,  but 
these  signs  are  bilateral,  and,  as  a  rule,  they  develop  without  active 
fever,  rusty  sputum,  or  herpes  in  a  patient  prostrated  by  some  long 
illness  accompanied  by  enfeeblement  of  the  heart  and  by  circulatory 
stasis  in  the  dependent  portions  of  the  lungs. 

In  acute  pulmonary  edema  there  is  usually  some  obvious  cardio- 
renal  defect  to  explain  the  suddenly  developing  respiratory  stress  and 
the  distinctive  serous,  frothy  expectoration.  The  physical  signs,  in 
contrast  to  those  of  pneumonia,  are  bilateral,  not  unilobar,  and  tend 
rapidly  to  spread  upward  over  both  lungs  from  the  bases;  vocal 
fremitus  and  respiratory  sounds  are  suppressed,  not  exaggerated; 
percussion  resonance  is  impaired,  not  abolished; -and  the  adventitious 
sounds  consist  of  various  sized  liquid  rales,  in  place  of  fine  vesicular 
crepitations  and  pleural  friction.  Fever  is  absent,  except  in  the  so- 
called  inflammatory  edema. 

In  differentiating  pulmonary  infarction  and  pneumonia  the  discovery 
of  a  source  of  embolism,  such  as  mitral  disease  or  femoral  phlebitis, 
is  a  valuable  diagnostic  asset.  Like  pneumonia,  infarction  gives 
rise  to  sudden  dyspnea,  cough,  pleural  pain,  hemoptysis,  and,  if  the 
infarcted  area  be  extensive,  to  physical  signs  of  a  dense  basic  infiltra- 
tion of  the  lung.  Unlike  pneumonia,  infarction  is  attended  by  mode- 
rate, if  any,  fever,  and  by  frankly  hemorrhagic  and  fluid  expectoration, 
while  the  consolidated  patch  is  sharply  circumscribed  and  does  not 
undergo  the  progressive  evolution  of  a  pneumonic  lesion.  Evidences 
of  pulmonary  abscess  or  gangrene  are  to  be  expected  when  the  infarc- 
tion is  due  to  an  infected  embolus. 


212  PHYSICAL   DIAGNOSIS 

Acute  diffuse  bronchitis,  in  the  exceptional  instance,  develops  most 
abruptly,  with  chill,  fever,  dyspnea,  and  even  hemoptysis,  hut  here 
the  resemblance  to  pneumonia  ends,  for  the  physical  signs  point 
conclusively  to  inflammation  of  the  tracheobronchial  tree,  without 
dulness  or  crepitations  at  the  bases  of  the  lungs. 

The  differentiation  of  croupous  pneumonia  from  catarrhal  pneu- 
monia, acute  pneumonic  phthisis,  and  pleural  effusion  is  considered 
in  connection  with  these  diseases.  (See  pp.  192,  216,  and  268.) 

Meningitis  is  counterfeited  by  certain  cases  of  pneumonia,  especially 
by  the  so-called  "cerebral  pneumonia"  of  children,  in  whom  the 
attack  is  ushered  in  by  a  convulsion,  headache,  restlessness,  delirium, 
and  a  variable  degree  of  cervical  rigidity.  Add  to  this  group  of 
symptoms  herpes,  leukocytosis,  and  arthritis,  and  a  highly  suggestive 
picture  of  cerebrospinal  meningitis  is  produced.  In  the  type  of 
pneumonia  under  discussion,  however,  such  a  train  of  events  means 
simply  an  intense  meningeal  congestion,  and  is  associated  with  the 
signs  of  lobar  consolidation,  not  uncommonly  at  the  apex.  True 
meningitis,  when  it  complicates  pneumonia,  ordinarily  develops  at 
the  height  of  the  febrile  stage,  and  is  attended  by  distinctive  symp- 
toms— delirium,  vomiting,  persistent  occipital  headache,  irrita- 
bility, tremor,  stupor,  and  painful  retraction  of  the  muscles  of  the 
neck  and  the  back.  The  muscular  reflexes  are  primarily  exaggerated, 
but  later  abolished,  and  in  some  instances  strabismus,  ptosis,  pupil 
changes,  and  various  paralyses  occur.  Kernig's  sign  (inability  to 
extend  the  leg  when  the  thigh  is  flexed  at  right  angles  to  the  trunk) 
is  of  practical  importance.  Lumbar  puncture  may  prove  conclusive, 
the  cerebrospinal  fluid  thus  obtained  showing  gross  changes,  cyto- 
logic  abnormalities,  and  bacteriologic  findings  distinctive  of  menin- 
geal inflammation  excited  by  the  pneumococcus,  meningococcus, 
streptococcus,  tubercle  bacillus,  or  other  microorganisms.  (See 
page  62.) 

Peritonitis  is  simulated  by  pneumonia  in  which  vomiting,  hyper- 
pyrexia,  abdominal  pain,  and  more  or  less  distention,  tenderness, 
and  rigidity  of  the  belly-wall  are  conspicuous  early  symptoms.  A 
clinical  picture  of  this  sort,  which  is  not  unusual  in  a  child,  may 
counterfeit,  according  to  the  locality  of  the  pain,  appendicitis,  gastric 
ulcer,  or  cholecystitis,  and  it  is  safe  to  regard  every  bellyache  in  a 
child  as  a  potential  sign  of  trouble  above  the  midriff.  Irritation  of 
the  pleural  filaments  of  the  lower  intercostal  nerves  is  responsible 
for  this  variety  of  reflected  abdominal  pain,  traceable  to  its  true 
source  by  an  analysis  of  the  patient's  clinical  history  and  by  physical 
examination  of  the  lungs,  which  ordinarily  reveals  pneumonia  of  the 
lower  lobe  or  lobes  and  wide-spread  pleurisy. 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM 


213 


CHRONIC   INTERSTITIAL  PNEUMONIA   (Fibroid  Pneumonia;    Fi- 
broid Lung;  Fibroid  Induration;  Pulmonary  Cirrhosis  or  Sclerosis) 

Clinical  Pathology. — Interstitial  pneumonia  is  a  chronic  inflam- 
mation of  the  pulmonary  connective  tissue,  attended  by  fibrous  over- 
growth and  subsequent  contraction  leading  to  permanent  sclerotic 
changes  in  the  bronchopulmonary  structure  (Fig.  99).  According 
to  the  conditions  prevailing  in  the  individual  case,  the  process  origi- 
nates in  the  peribronchial  tissues,  alveoli  and  their  walls,  interlobular 


Areas  of  consolidation 


Area  of  fibrosis 


Fig.  99. — Chronic  interstitial  pneumonia  (Jefferson  Hospital  Laboratories). 

septa,  or  pleura,  and  develops  subsequently  into  either  a  diffuse  or 
a  circumscribed  fibrosis  of  variable  extent. 

Diffuse  interstitial  pneumonia,  commonly  of  unilateral  distribution, 
but  exceptionally  implicating  both  lungs,  not  infrequently  follows 
bronchopneumonia,  and  begins  as  a  luxuriant  peribronchial  fibrosis 
spreading  through  the  interlobular  septa  to  the  alveolar  walls,  and 
ultimately  invading  an  entire  lobe,  or  even  the  whole  lung.  More 


214  PHYSICAL    DIAGNOSIS 

rarely  the  fibrosis  is  the  relic  of  a  faultily  resolved  croupous  pneumonia, 
in  which  organization  of  the  persistent  intravesicular  exudate  and 
a  fibrous  overgrowth  in  the  intervesicular  septa  combine  to  produce 
the  condition  termed  "gray  induration"  at  the  site  of  the  pneumonic 
infiltration.  In  other  instances  the  cirrhotic  changes  are  secondary 
to  plastic  inflammation  of  the  pleura,  whence  fibrous  bands  penetrate 
the  lung  by  way  of  the  septa  between  the  lobules  and  along  the  peri- 
bronchial  lymphatics;  or  a  pleural  thickening  and  contraction  may 
progressively  compress  the  adjacent  lung  and  set  up  interstitial 
changes  in  the  atelectatic  territory.  Compression  atelectasis,  as 
by  neoplasm  or  by  aneurism,  and  also  pulmonary  syphilis  are 
capable  of  initiating  a  more  or  less  diffuse  fibrosis  of  the  lungs. 
The  cirrhotic  lesions  arising  primarily  from  irritation  by  dusts 
are  considered  in  connection  with  Pneumokoniosis  (p.  252),  and 
the  fibrosis  due  to  tuberculosis  is  described  under  Fibroid  Phthisis 
(P-  234). 

The  cirrhotic  areas  consist  of  dense,  pigmented  collections  of  gray 
cicatricial  tissue  disseminated  throughout  the  organ,  commonly  by 
peribronchial  radiations  between  the  lobules  and  the  lobes,  and  in 
the  extreme  case  converting,  by  contraction  of  the  fibrous  overgrowth, 
the  lobe  or  even  the  lung  into  an  airless,  sclerotic  mass  of  extraordi- 
narily small  volume.  At  autopsy  a  lung  thus  damaged  may  be  reduced 
to  a  compact,  indurated  mass  of  fibroid  material  the  size  of  a  cante- 
loupe,  lying  against  the  spinal  column.  In  consequence  of  this 
unilateral  shrinkage  the  thorax  on  the  fibroid  side  is  strikingly  con- 
tracted and  otherwise  distorted  (see  Fig.  45),  and  the  heart,  which  is 
hyper trop hied,  especially  on  the  right  side,  is  drawn  toward  the  focus 
of  the  cirrhosis,  along  with  the  other  mediastinal  contents.  The 
bronchi  are  generally  dilated,  and  the  air-vesicles  are  quite  oblite- 
rated in  the  fibroid  areas,  while  elsewhere  both  these  structures 
show  a  variable  degree  of  catarrhal  inflammation.  In  the  non- 
fibroid  parts  of  the  affected  lung  and  throughout  the  other  lung 
compensatory  emphysema  develops,  and  the  pleural  surfaces  are 
thickened  and  adherent,  in  cases  of  pleurogenous  origin,  though 
they  may  escape  injury  in  primary  pulmonary  fibroses. 

Aside  from  the  foregoing  lobar  type,  there  are  instances  in  which  the 
fibrosis,  though  extensive,  conforms  more  closely  to  a  lobular  dis- 
tribution, the  process  consisting  essentially  of  a  commingling  of 
numerous  indurated  patches  and  intervening  areas  of  emphysema. 
This  variety  of  interstitial  pneumonia,  inasmuch  as  it  is  characterized 
by  multiple  discrete  lesions  situated  usually  at  the  bases  and  deep 
within  the  lungs,  does  not  ordinarily  cause  the  conspicuous  medias- 


DISEASES    OF   THE   BRONCHOPULMONARY   SYSTEM        215 

tinal  displacement  and  chest  deformity  so  distinctive  of  a  massive, 
confluent  cirrhosis. 

Circumscribed  interstitial  pneumonia,  or  local  fibrosis,  is  sharply 
restricted  to  a  limited  area,  and  arises  in  consequence  of  some  local 
damage  to  the  pulmonary  structure.  The  process  is  to  be  regarded 
as  virtually  reparative  in  character,  for  its  tendency  is  to  encompass 
the  primary  injury  with  an  impermeable  capsule  of  contracting  con- 
nective tissue,  and  thus  to  stay  the  spread  of  infection,  if  not,  indeed, 
to  extinguish  the  lesion  completely.  Fibrous  scars  of  this  sort  mark 
the  sites  of  structural  injuries  of  the  lungs  due  to  factors  such  as  tuber- 
culosis, gumma,  abscess,  gangrene,  actinomycosis,  echinococcus  cyst, 
and  neoplastic  growths. 


Fig.  too. — Radiograph  of  chronic  interstitial  pneumonia  (cf.  Fig.  70).     Note  dense 
shadows  of  fibrosis  through  the  right  lung.     (Plate  by  Dr.  W.  F.  Manges.) 

Physical  Signs. — Since  the  physical  signs  of  interstitial  pneumonia 
are  essentially  those  of  its  clinical  counterpart,  fibroid  phthisis,  their  de- 
tailed discussion  will  be  taken  up  in  connection  with  this  form  of  tuber- 
culosis. (See  p.  235.)  It  suffices  here  to  note  that  the  clinical  picture  is 
made  up  of  thoracic  distortion  and  restricted  respiration  on  the  affected 
side,  with  enlargement  and  overaction  of  the  opposite  side;  that  the 
heart  is  displaced  toward  the  site  of  the  lesion  and  the  anterior  pul- 
monary borders  may  be  retracted  from  the  precordia;  that  over  the 
cirrhotic  areas  increased  vocal  fremitus,  dulness  or  flatness,  and  either 


2l6  PHYSICAL   DIAGNOSIS 

suppressed  or  harsh  breathing  are  found,  while  the  overdistended 
monic  second  sound,  with  the  subsequent  development  of  the  mur- 
mur of  tricuspid  relative  insufficiency,  indicates  the  strain  upon,  and 
the  inevitable  failure  of,  the  right  ventricle. 

Diagnosis. — Upon  the  foregoing  signs,  plus  a  story  of  cough, 
dyspnea,  and  mucopurulent,  perhaps  bloody,  expectoration,  per- 
sisting for  many  years  without  notably  impairing  the  subject's  strength, 
the  diagnosis  of  chronic  interstitial  pneumonia  is  based,  and  the 
opinion  thus  formed  is  made  still  more  tenable  when  there  is  a  past 
territories  afford  hyperresonance  and  exaggerated  breath-sounds. 
In  pleurogenous  fibrosis  friction  is  to  be  looked  for,  and  over  areas 
of  great  pleural  thickening,  deadening  of  the  voice  and  respiratory 
sounds.  The  cavernous  signs  of  bronchiectasis  are  sometimes 
demonstrable.  Accentuation  and  ultimate  enfeeblement  of  the  pul- 
history  of  pneumonia,  pleurisy,  syphilis,  or  local  damage  to  the 
lung,  to  account  for  the  initial  cirrhotic  changes.  In  a  doubtful 
case  the  x-ra.y  generally  affords  a  certain  means  of  diagnosis  (Fig. 
100).  The  differentiation  of  pure  pulmonary  cirrhosis  from  so-called 
fibroid  phthisis,  which  is  not  always  possible  when  positive  bac- 
teriologic  findings  and  a  clear  history  are  wanting,  is  referred  to 
under  the  latter  affection.  (See  p.  234.) 

ACUTE  PNEUMONIC  PHTHISIS   (Phthisis  Florida;  Galloping  Con- 

sumption) 

Clinical  Pathology. — This  acute  type  of  pulmonary  tuberculosis, 
popularly  known  as  "galloping  consumption,"  consists  of  a  rapidly 
spreading  caseous  pneumonia  or  bronchopneumonia,  which  is  com- 
monly secondary  to  a  primary  apical  focus  of  infection  (Fig.  101). 
The  vesicles  and  bronchioles  are  the  seat  of  intense  inflammatory 
changes,  and  are  filled  with  an  inflammatory  exudate  which, 
owing  to  its  tuberculous  character,  does  not  readily  undergo 
softening  and  expulsion,  but  becomes  caseated;  the  vesicular  and 
bronchiolar  walls  in  the  affected  areas  are  infiltrated  and  thick- 
ened, and  their  blood-supply  is  obliterated.  With  the  spread  of  the 
infection  from  its  original  site  to  adjacent  vesicles  and  bronchioles, 
there  is  rapid  implication  of  the  entire  lobule,  whence  the  process 
spreads  to  adjacent  lobules,  either  by  coalescence  of  their  lesions  or 
by  direct  extension.  The  size  of  these  patches  of  tuberculous  con- 
solidation varies  greatly  in  the  individual  case,  according  to  the 
virulence  of  the  infection  and  the  resistance  of  the  subject.  In  the 
so-called  pneumonic  type  of  the  disease  there  is  a  diffuse,  apparently 
uniform  consolidation  of  a  lobe  or  even  of  an  entire  lung,  the  changes 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM 


closely  resembling  those  of  croupous  pneumonia,  both  in  their  lobar 
distribution  and,  it  may  be,  in  the  fibrinous  character  of  the  alveolar 
exudate.  In  other  cases,  those  of  the  bronchopneumonic  type,  the 
lesions  are  more  widely  disseminated,  and  conform,  both  in  their 
lobular  distribution  and  in  the  presence  of  a  catarrhal  exudate,  to 
the  changes  produced  by  bronchopneumonia.  In  their  early  stages 
the  tuberculous  foci  are  recognized  as  white  or  grayish  areas  showing, 


Diffuse  infiltratioi 
and  softening 


Infarct 


Cavity 
Fig.  101. — Acute  pneumonic  phthisis  (Jefferson  Hospital  Laboratories). 

on  microscopic  examination,  the  histologic  structure  of  tubercles; 
in  their  later  stages,  as  caseation  progresses,  their  color  becomes 
more  and  more  yellow;  and  ultimately,  owing  to  softening,  secondary 
infection  and  discharge  of  the  contents  of  the  tubercles,  the  lung 
may  become  riddled  with  cavities,  generally  of  small  or  moderate 
size.  Isolated  miliary  tubercles  also  are  commonly  demonstrable, 
especially  toward  the  apices  and  beneath  the  pleura,  which  is  generally 
thickened  and  covered  with  a  fibrinous  or  a  caseous  exudate.  The 


2l8  PHYSICAL   DIAGNOSIS 

bronchi  are  more  or  less  acutely  inflamed,  enlargement  of  the  bron- 
chial glands  is  virtually  constant,  and  the  lungs  show  atelectatic  and 
emphysematous  changes.  Pyopneumothorax,  from  perforation  of 
the  pleura  by  a  tuberculous  nodule,  is  a  complication  of  considerable 
frequency. 

Physical  Signs. — Pneumonic  Type. — The  physical  signs  are 
essentially  those  of  lobar  consolidation,  commonly  of  an  upper  lobe, 
and  exceptionally  of  an  entire  lung.  On  inspection,  it  is  seen  that  the 
patient's  face  bears  the  pneumonic  flush  and  that  the  breathing  is 
hurried;  or  there  may  be  urgent  dyspnea,  with  more  or  less  bluish 
pallor  and  inspiratory  gaping  of  the  nostrils.  The  spit-cup  is  likely 
to  contain  viscid  mucoid  material  or  typically  rusty  sputum,  in  which 
tubercle  bacilli  may  or  may  not  be  found.  Palpation  yields  exag- 
gerated vocal  fremitus  over  the  consolidation,  and  sometimes  reveals 
areas  of  restricted  motility  not  noticed  on  inspection.  Percussion 
shows  dulness,  preceding  the  development  of  which  the  percussion 
sound  may  have  been  decidedly  hyperresonant.  On  auscultation 
over  the  affected  area  enfeebled  breath-sounds  and  vesicular  crepi- 
tations are  heard  in  the  early  stages,  succeeded  by  bronchovesicular 
and  finally  by  bronchial  breathing,'  and  by  intense  bronchophony, 
as  the  consolidation  progresses.  These  physical  signs  are  practically 
those  of  ordinary  croupous  pneumonia,  but,  unlike  them,  they  fail 
to  clear  up,  critically,  at  the  end  of  a  five-  or  ten-day  period.  On  the 
contrary,  the  consolidated  areas  soon  begin  to  soften,  to  ulcerate,  and 
to  become  excavated,  in  consequence  of  which  cavity  signs  supervene 
and  the  sputum  is  charged  with  elastic  fibers  and  teems  with  tubercle 
bacilli.  This  state  of  affairs  may  continue  for  ten  or  twelve  weeks 
before  the  patient  dies,  but  more  commonly  vital  damage  to  the  lungs 
is  accomplished  within  six  or  eight  weeks,  or,  in  the  exceptionally  ful- 
minant case,  within  a  fortnight.  Occasionally  the  acute  progress 
of  the  process  is  modified,  and  the  disease  runs  its  subsequent  course 
as  a  chronic  pulmonary  tuberculosis,  generally  of  the  ulcerative  type. 

Bronchopneumonic  Type. — This  form  of  acute  phthisis,  which  is 
generally  bilateral,  is  ushered  in  with  predominant  signs  of  an  acute 
bronchiolitis — numerous  sibilant  and  subcrepitant  rales  scattered 
over  both  lungs.  As  the  smaller  tubes  fill  with  cheesy  material  and 
the  vesicles  of  the  communicating  lobules  undergo  catarrhal  changes, 
definite  evidences  of  the  tuberculous  bronchopneumonia  are  apparent. 
On  inspection,  the  patient's  dyspnea,  cyanosis,  and  panting  respira- 
tion attest  the  stress  of  his  fight  for  oxygen.  Palpation  discovers 
scattered  patches,  especially  apical,  of  increased  vocal  fremitus, 
over  which  auscultation  affords  bronchovesicular  or  even  tubular 
breathing,  bronchophony,  and  subcrepitant  and  crepitant  rales. 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        2 19 

Jurgensen's  sign — the  delicate  crepitation  of  pleural  tubercles — is 
sometimes  demonstrable.  These  signs,  instead  of  abating  after  two 
or  three  weeks,  as  is  the  rule  in  non- tuberculous  bronchopneumonia, 
persist  and  are  subsequently  overshadowed  by  evidences  of  softening 
and  excavation  of  the  caseous  foci.  Sometimes  the  picture  of  the 
typhoid  state  supervenes,  and  the  subject  survives  but  three  or  four 
weeks;  but  in  other  instances,  despite  the  gravity  of  the  disease,  an 
extraordinary  remission  occurs  after  the  patient  has  been  prostrated 
for  several  weeks,  the  physical  signs  becoming  transformed  into 
those  of  chronic  phthisis  with  multiple  cavities  and  considerable 
fibrosis. 

Diagnosis. — For  a  time  croupous  pneumonia  may  be  faithfully 
counterfeited  by  acute  phthisis  of  the  pneumonic  type,  owing  to  its 
sudden  onset,  initial  chill,  high  fever,  cough,  and  evidences  of  lobar 
consolidation.  At  an  early  period  there  may  be  absolutely  no  means 
of  differentiation,  although  primary  implication  of  an  apex,  slow 
extension  of  the  consolidation,  and  a  remittent  type  of  fever  are  more 
suggestive  of  tuberculous  than  of  pneumococcus  pneumonitis.  The 
early  detection  of  tubercle  bacilli  in  the  sputum  is,  of  course,  all 
important,  but  often  this  is  not  possible,  and  the  same  is  apparently 
true  of  the  ophthalmotuberculin  reaction.  The  disease  runs  its 
course  unchecked  past  the  time  of  a  pneumonic  crisis  without  under- 
going a  critical  defervescence,  but,  on  the  contrary,  becomes  more 
and  more  alarming,  the  high  fever  persisting  and  showing  greater 
fluctuations,  the  pulse-rate  quickening,  drenching  sweats  occurring, 
and  the  sputum,  previously  rusty  or  mucopurulent,  becoming  of 
yellowish  and  greenish  hue  and  laden  with  tubercle  bacilli  and  perhaps 
bits  of  elastic  fibers.  The  infection  now  appears  in  its  true  light, 
especially  as  by  this  time  the  patient's  emaciation  and  toxemia  are 
pronounced  and  the  lungs  show  unmistakable  signs  of  softening  over 
the  areas  primarily  consolidated. 

In  the  bronchopneumonic  type  the  differentiation  from  non- 
tuberculous  bronchopneumonia  is  frequently  called  for,  since  the  chief 
early  symptoms  are  urgent  dyspnea,  cough,  a  chill  or  repeated  rigors, 
high  fever,  a  rapid  pulse,  and  the  physical  signs  of  diffuse  bronchioli- 
tis.  In  some  cases,  however,  hemoptysis  is  the  initial  symptom,  and 
it  is  possible  to  find  tubercle  bacilli  early;  but  generally  these  are  later 
signs,  and  one  must  wait  for  softening  of  the  tuberculous  foci,  to  be 
sure  of  the  diagnosis,  though  the  progressive  emaciation  of  the  patient 
gives  no  uncertain  hint.  A  tuberculous  family  history  and  a  recent 
attack  of  measles  or  of  pertussis  are  in  favor  of  the  tuberculous  char- 
acter of  any  obscure  bronchopneumonia. 


220  PHYSICAL    DIAGNOSIS 

The  wide-spread  bronchitis  of  certain  cases  of  enteric  fever  may 
require  discrimination,  but  in  this  disease  the  development  of  an 
orderly  sequence  of  typhoid  symptoms,  plus  the  lack  of  distinctive 
tuberculous  physical  signs,  will  effectually  settle  the  question. 

CHRONIC  ULCERATIVE   PHTHISIS  (Slow  Consumption) 

Clinical  Pathology. — This  form  of  phthisis,  which  is  primarily 
a  chronic  tuberculous  pneumonitis,  serves  to  illustrate  every  possible 
phase  of  damage  which  the  lungs  may  suffer  from  invasion  by  the 
tubercle  bacillus  and  by  associated  secondary  bacterial  infection. 
In  the  well-advanced  case  a  most  diverse  group  of  lesions  develops, 
ranging  from  minute  miliary  granules  to  extensive  areas  of  destruction 
due  to  excavation  and  to  fibroid  overgrowth.  To  such  a  condition 
the  lay  term,  "consumption  of  the  lungs,"  is  singularly  applicable 
(Fig.  102). 

In  the  majority  of  cases  there  can  be  no  question  that  the  infec- 
tion is  of  bronchogenic  origin,  arising  in  consequence  of  the  inhalation 
of  tubercle  bacilli,  which  lodge  in  the  terminal  bronchi  or,  less 
commonly,  in  the  larger  bronchial  tubes.  In  the  first  instance  the 
bacteria  directly  excite  a  caseous  bronchopneumonia  and  also  pene- 
trate the  bronchioalveolar  epithelium,  thus  initiating  the  growth 
and  distribution  of  tuberculous  foci  in  the  surrounding  connective 
tissue.  These  two  lesions,  though  theoretically  distinct,  rapidly 
merge  into  a  single  focus,  whence  dissemination  of  the  infection  to 
other  parts  of  the  lungs  is  effected  by  the  lymphatic  vessels  and  by 
secondary  aspiration  of  tuberculous  material  into  the  finer  bronchial 
twigs.  Exceptionally,  the  initial  phthisical  lesion  is  ingrafted  upon 
a  preexisting  inflammation  of  the  larger  bronchi,  which  become  the 
seat  oi  tuberculous  inflammation  and  ulceration,  whence  the  bron- 
chiolar  and  alveolar  structures  become  secondarily  infected,  by  aspira- 
tion. The  bronchial  glands  are  likely  to  be  the  seat  of  miliary  and 
caseous  lesions,  terminating  perhaps  by  calcification  or  by  suppura- 
tion, often  with  the  most  disastrous  results. 

Aside  from  its  origin  by  inhalation,  pulmonary  tuberculosis  may 
also  arise  from  infection  through  the  alimentary  canal,  for  tubercle 
bacilli  swallowed  and  taken  into  the  intestines  are  able  to  penetrate, 
without  exciting  a  local  lesion,  the  intact  mucosa  of  the  gut,  and  are 
carried  hence,  by  the  lacteals  and  the  thoracic  duct,  ultimately  to 
lodge  in  the  capillaries  of  the  lungs.  Children  are  especially  sus- 
ceptible to  infection  along  this  path,  which,  though  traveled  in  a 
considerable  proportion  of  all  cases  of  phthisis,  cannot  be  regarded  as 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         221 

the  only  portal  of  entry,  to  the  exclusion  of  the  older  inhalation 
theory  of  infection  via  the  air-passages. 

As  tuberculous  foci  age,  more  and  more  of  the  lung  tissue  becomes 
invaded  by  the  disease,  and  less  and  less  distinction  is  possible  between 
the  tubercles  and  the  adjacent  spots  of  caseous  pneumonia.  Exces- 
sive proliferation  of  connective  tissue  is  the  rule  in  the  neighborhood 
of  the  tuberculous  lesions,  and  in  many  such  areas  this  reparative 
process  is  actually  obliterative,  in  that  it  finally  converts  the  tubercles 
into  a  dense  cicatrix,  or  encapsulates  them  with  a  thick,  fibrous  wall, 

Small  cavities 


Large  cavity 


Fig.  102. — Chronic  ulcerative  phthisis  (Jefferson  Hospital  Laboratories). 

which  later  becomes  still  more  impermeable  through  calcification. 
A  cheesy  spot  thus  thoroughly  inclosed  or  obliterated  is,  to  all  intents 
and  purposes,  healed,  but  should  the  fibrous  envelop  be  too  delicate, 
the  infective  material,  even  after  a  long  period  of  latency,  may  pene- 
trate the  barrier  and  thus  light  up  afresh  the  disease.  Hand  in  hand 
with  these  reparative  changes  the  degenerative  necroses  of  the  tuber- 
cles progress,  as  shown  by  their  tendency  to  undergo  cheesy  softening, 
liquefaction,  and  ulceration,  the  final  result  being  the  formation  of 


222  PHYSICAL    DIAGNOSIS 

cavities,  many  of  which  find  a  bronchial  outlet  by  ulcerative  extension. 
The  wall  of  such  a  cavity  is  formed  of  a  fibrous  overgrowth  lined  by 
a  pyogenic  membrane,  and  its  contents  consist  of  foul  mucopurulent 
secretion  swarming  with  both  pyogenic  and  tubercle  microorganisms 
and  laden  with  caseous  masses,  elastic  tissue,  degenerate  epithelium, 
and  blood-  and  pus-cells.  A  cavity  may  enlarge  by  the  process  of 
chronic  ulcerative  erosion  kept  up  by  the  combined  action  of  pyogenic 
cocci  and  tubercle  bacilli;  and  several  moderate-sized  cavities  may 
fuse  into  a  single  large  excavation,  or  they  may  form  a  chain 
of  communicating  chambers.  Some  cavities  are  but  one  or  two 
centimeters  in  diameter,  while  others  destroy  practically  an  entire 
lung.  A  blood-vessel  that  has  escaped  thrombotic  obliteration  within 
a  cavity  is  to  be  regarded  as  a  possible  source  of  serious,  even  fatal, 
hemorrhage,  the  blood  issuing  either  from  a  breach  eroded  in  the 
vessel-wall,  or  from  the  rupture  of  an  aneurismal  dilatation  of  a 
vessel  (Rasmussen's  aneurism)  in  the  lining  membrane  of  the  cavity 
or  bridging  it  from  wall  to  wall.  It  is  obvious  that  in  a  cavity  with  no 
bronchial  outlet  such  a  hemorrhage  is  not  betrayed  by  hemoptysis, 
this  accident  being  a  so-called  "concealed  hemorrhage"  of  phthisis. 
Aside  from  the  foregoing  types  of  cavity,  there  are  those  of  bronchiec- 
tatic  origin,  due  to  the  dilatation  of  small  bronchi  weakened  by 
tuberculous  ulceration  and  distended  by  accumulations  of  secretion 
pent  up  within  the  diseased  tubes.  These  have  been  referred  to 
in  the  discussion  of  bronchiectasis.  (See  Fig.  93). 

The  pleura  in  a  case  of  chronic  ulcerative  phthisis  rarely,  if  ever, 
escapes  injury,  either  in  the  form  of  a  simple  dry  pleurisy  with  adhe- 
sion and  thickening,  or  as  a  tuberculous  invasion  by  miliary  and 
caseous  foci.  Pleural  effusions  and  pyopneumothorax  are  likewise 
to  be  reckoned  with  in  numerous  instances.  The  non-tuberculous 
pulmonary  tissue  is  generally  overdistended  in  its  endeavor  vicariously 
to  offset  the  crippling  effects  of  the  phthisis,  and  in  many  areas 
atelectasis  and  compression  of  the  lung  are  apparent. 

About  i  per  cent,  of  all  cases  of  pulmonary  tuberculosis  is 
attended  by  chronic  valvular  disease  of  the  heart,  which  only  ex- 
ceptionally is  of  tuberculous  nature,  and  the  latter  is  true  also  of 
pericarditis,  a  rare  complication  usually  arising  secondarily  by  ex- 
tension from  the  pleura  or  from  a  cavity.  Tuberculosis  of  the  heart 
muscle  is  exceptional,  but  myocardial  degeneration  is  common. 
The  size  of  the  heart  is  commonly  smaller  than  normal  in  phthisical 
subjects,  and  this  change  is  variously  attributed  to  factors  such  as 
congenital  anomalies,  general  cardiovascular  hypoplasia,  and  the 
effects  of  habitual  inspiratory  restriction.  Right-sided  dilatation 
occurs  as  the  result  of  long-standing  pulmonary  fibrosis  and  asso- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        223 

ciated  changes  which  strain  the  right  ventricle;  and  in  such  cases 
loss  of  compensation  and  the  onset  of  cardiac  failure  hastens  the 
progress  of  the  pulmonary  infection. 

Mitral  regurgitation  is  by  far  the  commonest  valvular  defect  in 
phthisical  patients.  It  has  little  or  no  effect  upon  the  pulmonary 
lesion,  although  if  compensation  be  good  it  may  retard  its  progress 
(Lawrason  Brown).  Pulmonary  stenosis,  in  that  it  causes  per- 
sistent pulmonary  anemia,  predisposes  to  phthisis;  while  the  effect 
of  mitral  stenosis,  which  sets  up  a  constant  congestion  of  the 
lungs  and  concentrates  in  them  the  immunizing  agents  of  the 
blood,  is  supposed  to  be  more  or  less  antagonistic.  Aortic  disease 
is  more  commonly  associated  with  latent  than  with  active  types 
of  pulmonary  tuberculosis. 

In  incipient  phthisis  lowered  blood-pressure  with  acceleration  of 
the  pulse-rate  is  the  rule,  and  as  the  disease  advances  both  signs 
grow  more  conspicuous,  owing  to  degeneration  of  the  myocardium 
from  the  effect  of  the  tuberculous  virus. 

Aside  from  the  secondary  infections  that  may  attack  various 
parts  of  the  respiratory  tract,  the  important  complications  of 
phthisis  include  tuberculosis  of  the  intestines,  kidneys,  lymphatic 
glands,  meninges,  and  ischiorectal  abscess. 

Usually  the  initial  lesion  of  chronic  ulcerative  phthisis  develops 
in  the  upper  lobe  of  one  lung  (most  commonly  the  right)  at  a  point 
one  or  one  and  one-half  inches  (2.5  to  3.75  cm.)  below  its  extreme 
apex  (Kingston  Fowler) ,  whence  the  process  tends  to  spread  down- 
ward on  the  same  side,  and  later  to  the  apex  of  the  opposite  lung, 
as  the  result  of  which  method  of  extension  the  apical  lesions  are  likely 
to  be  older  and  more  advanced  than  those  of  the  bases.  Exception- 
ally, the  starting-point  of  the  disease  is  in  a  lower  lobe,  such  instances 
occurring  more  commonly  in  children  than  in  adults.  Clinically, 
the  earliest  physical  evidences  of  phthisis  are  demonstrable  either 
anteriorly,  just  below  the  center  of  the  clavicle  and  below  the  outer 
third  of  this  bone  in  the  first  and  second  interspaces,  or  posteriorly 
in  the  supraspinous  fossa.  Infection  of  the  lower  lobe  begins  poster- 
iorly at  a  point  about  i£  inches  (3.75  cm.)  below  its  summit  (Kingsley), 
the  physical  signs  of  such  an  invasion  being  found  at  a  spot  opposite 
the  fifth  thoracic  vertebra,  whence  they  spread  downward  and  out- 
ward along  the  line  of  the  vertebral  border  of  the  scapula,  when  it 
is  elevated  by  having  the  subject  place  the  hand*  upon  the  opposite 
shoulder  with  the  elbow  raised  above  this  level. 

Although  no  case  of  phthisis  can  be  expected  to  run  a  clinical 
course,  divisible  into  fixed,  well-defined  stages,  it  seems  best,  when 
examining  a  suspected  case  of  this  disease,  to  have  in  mind  certain 


224  PHYSICAL    DIAGNOSIS 

arbitrary  periods  of  the  infection,  so  as  intelligently  to  correlate  the 
physical  signs  with  the  underlying  pulmonary  lesions.  It  is,  therefore, 
convenient  to  divide  the  disease  into  three  periods,  which,  it  is  per- 
fectly obvious,  must  overlap,  merge,  and  variously  dominate  the 
clinical  picture,  according  to  the  peculiarities  of  the  process  in  the 
individual  patient.  The  first  period,  which  includes  the  stage  of 
initial  tuberculous  deposits,  may  exist  for  some  time  and  yet  afford 
no  definite  physical  signs;  and  in  this  category  belong  the  so-called 
"incipient"  cases,  with  suspicious  histories  and  negative  or  trifling 
signs,  as  well  as  those  with  clear  evidences  of  one  or  more  circum- 
scribed, limited  areas  of  infiltration.  The  second  period,  correspond- 
ing to  the  wider  dissemination  and  softening  of  the  infiltrations, 
comprises  cases  with  single  or  multiple  lesions  undergoing  degener- 
ative changes,  the  objective  symptoms  of  which  are  conspicuous. 
The  third  period,  that  of  cavity  formation,  affords  signs  of  pulmonary 
excavation  and  extensive  fibrosis,  with  extension  of  the  infiltration 
and  softening  originally  determined. 

Physical  Signs. — Inspection. — In  incipient  cases  one  must  often 
be  content  to  gain  information  from  minor  stigmata  rather  than  from 
characteristic  hall-marks  of  the  disease.  Typical  illustrations  of 
such  stigmata  have  been  perpetuated  in  Botticelli's  pallid  angels, 
and  in  Rosetti's  and  Burne- Jones's  lanky  beauties,  whose  wistful, 
pained  faces,  long,  slender  necks,  and  stooped,  flat-chested  trunks 
are  highly  suggestive  of  early  phthisis.  As  Iwai  has  shown,  super- 
numerary breasts  are  twice  as  common  in  phthisical  as  in  healthy 
women.  The  characteristics  of  the  phthisical  or  alar  type  of  thorax 
will  be  found  in  a  foregoing  section.  (See  p.  78.)  In  this  con- 
nection it  is  interesting  to  note  that  Rothschild's  sign  (preternatural 
flattening  and  mobility  of  the  sternal  angle)  is  frequently  demon- 
strable long  before  the  first  signs  of  infiltration  appear.  Ankylotic 
rigidity  of  the  spinal  column,  especially  of  the  thoracic  and  lumbar 
segments  (Lorenz's  sign),  also  is  found  in  a  considerable  percentage 
of  patients  with  incipient  phthisis. 

Progressive  loss  of  weight  is  a  prominent  early  finding,  which,  as 
the  disease  advances,  becomes  correspondingly  more  conspicuous, 
the  emaciation  sometimes  attaining  a  most  extraordinary  degree. 
(See  Fig.  25,  p.  79.)  In  some  persons  phthisis  may  be  active  for  a  pro- 
longed period  without  apparently  making  inroads  upon  the  general 
health  and  nutrition.  A  striking  phase  of  the  present  European 
war  is  the  physical  fitness  and  ability  for  stress  shown  by  the  large 
number  of  tuberculous  soldiers  among  the  armies  engaged.  Guil- 
haud  even  goes  so  far  as  to  describe  a  form  of  phthisis  characterized 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         225 

by  obesity,  regarding  it  as  readily  curable  and  not  incompatible 
with  longevity. 

The  trained  eye  appreciates  the  pertinence  of  the  tuberculous 
facies;  an  oval  face,  with  delicate  or  pinched  features;  bright,  ap- 
pealing eyes,  with  dilated,  perhaps  unequal,  pupils  and  snow-white 
scleras;  and,  as  the  disease  progresses,  respiratory  dilatation  of 
the  nasal  alae  and  bright-red  hectic  flushes  upon  either  cheek 
(Fig.  103).  Gee's  trenchant  remark,  "we  should  never  see  anemia 
without  thinking  of  phthisis,"  should  serve  as  a  maxim  for  daily 
use  in  dealing  with  chest  cases,  although  blood  deterioration 
ordinarily  does  not  occur  until  malnutrition  and  sepsis  have  long 
been  at  work. 


- 

Fig.  103. — The  phthisical  facies  (Jefferson  Hospital). 

Incipient  apical  disease  is  early  betrayed  by  deficient  expansion 
and  flattening  of  one  infraclavicular  space,  the  former  defect 
usually  being  more  easily  recognized  by  palpation  than  by  in- 
spection (v.  i.}.  Lagging  or  complete  respiratory  immobility  of 
the  acromion  process  on  the  affected  side  is  another  early  sign  of 
real  value.  Diminished  pulmonary  elasticity  plus  spasmodic  mus- 
cular contraction  accounts  for  these  early  physical  signs,  and  if 
persistent  the  combined  factors  lead  to  actual  degeneration  of  the 
muscles  affected,  according  to  Pottenger's  studies.  The  trapezius 
and  the  sternocleidomastoid  muscles  are  notably  smaller,  softer, 
and  shorter  on  the  affected  side  in  unilateral  apical  lesions. 

As  softening  and  fibrosis  increase  the  neck  apparently  lengthens, 
the  supraclavicular  and  infraclavicular  regions  deepen  conspicu- 
ously, and  the  clavicles  become  abnormally  prominent;  the  inter- 
spaces sink  in,  the  ribs  overlap,  the  scapula  on  the  affected  side 


226  PHYSICAL   DIAGNOSIS 

tilts  outward,  and  circumscribed  areas  of  immobility,  flattening, 
and  retraction  appear  upon  the  chest-wall,  the  expansion  of  which 
progressively  diminishes  as  the  result  of  the  pulmonary  destruc- 
tion and  the  pleural  pain.  These  changes,  consisting  essentially 
of  reflex  muscle  spasm  and  atrophy,  are  largely  attributable  to 
disorders  of  the  thoracic  sympathetic  ganglion  and  to  irritation 
of  the  vagus,  the  brachial  plexus,  and  the  phrenic  and  intercostal 
nerves  (Pomeroy;  Balint;  Jessen).  In  extensive  unilateral  lesions 
the  opposite  half  of  the  thorax  may  be  vicariously  overdistended. 

More  or  less  restriction  of  Litten's  diaphragm  shadow  on  the 
affected  half  of  the  thorax  may  be  evident,  generally  in  consequence 
of  pleural  pain;  and  reversal  of  the  physiologic  respiratory  type  is 
a  common  anomaly  of  breathing  in  incipient  tuberculous  deposits. 

A  diffuse  cardiac  impulse,  visible  in  the  second,  third,  and  fourth 
left  interspaces,  is  commonly  found  in  advanced  tuberculosis  of  the 
left  apex,  in  consequence  of  fibrous  retraction  of  the  lappet  of  lung 
from  its  normal  site  between  the  heart  and  the  thoracic  wall.  Dis- 
placement of  the  apex  to  either  side  (more  frequently  to  the  left) 
occurs  very  frequently,  as  the  result  of  either  traction  or  pressure. 

Not  infrequently  a  delicate  tracery  of  small  venules  courses  over 
the  lower  part  of  the  anterior  chest-wall,  and  many  phthisical  sub- 
jects are  disfigured  by  a  downy  growth  of  hair,  by  dirty  brownish 
patches  of  tinea  versicolor,  especially  upon  the  back,  and  by  chloasmic 
discoloration  (chloasma  phthisicorum)  of  the  face.  In  tubercular 
children  with  a  tuberculous  family  history  Gibson  has  noted  the 
frequent  occurrence  of  numerous  visible  venules  upon  the  chest  and 
face,  associated  with  undue  prominence  of  one  or  both  jugulars, 
the  vessels  thus  overdistended  failing  to  show  a  normal  inspiratory 
collapse.  In  apical  tuberculosis  a  collection  of  delicate  red  or  purple 
lines  is  commonly  observed  in  the  skin  over  the  apex  of  the  lung — the 
"striae  vasculares"  of  Francke,  attributed  to  permanent  engorge- 
ment of  the  cutaneous  blood-vessels  due  to  toxins  derived  from  an 
underlying  focus  of  pulmonary  infection.  Lombardi  has  des- 
cribed as  an  early  sign  of  apical  phthisis  the  formation  of  small 
bluish  varicosities  near  the  lower  cervical  and  the  upper  thoracic 
vertebral  spines,  and  Sabourin  has  noted  depressed  ecchymotic 
spots  in  the  dorsolumbar  regions.  The  association  of  zona  and  of 
erythema  nodosum  with  phthisis  is  a  well-known  clinical  sign. 

Clubbed  fingers,  and  perhaps  true  examples  of  Marie's  osteo- 
arthropathy,  are  familiar  findings  during  the  later  stages  of  the 
disease.  (Seep.  121.) 

Since  tuberculous  lesions  produce  z-ray  shadows  corresponding 
to  their  location,  size,  and  density,  the  use  of  the fluoroscope.  and  the 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        227 

radiograph  is  of  real  value  in  the  diagnosis  of  phthisis,  as  well  as  in 
tracing  its  progress.  In  incipient  cases  haziness  or  mottling  of  an 
apex  is  shown  by  the  fluoroscope,  and  in  some  instances  a  more  or 
less  disseminated  darkening  over  the  greater  extent  of  the  diseased 
lobe.  Sometimes  the  shadows  cast  by  a  group  of  enlarged  bron- 
chial glands  give  the  first  clue  to  the  tuberculous  process.  The 
movement  of  the  diaphragm  is  more  restricted  on  the  affected  than 
on  the  sound  side  (Williams' s  sign),  and,  even  in  very  early  cases, 
inspiratory  traction  of  the  heart  toward  the  diseased  lung  may  be 
recognized.  The  "cough  phenomenon,"  or  the.  lightening  of  an 


Fig.  104. — Radiograph  of  phthisis  (cf.  Fig.  7°).     Early  stage,  showing  apical  infiltra- 
tion and  glandular  lesions.     (Plate  by  Dr.  W.  F.  Manges.) 

apical  shadow  as  the  subject  coughs,  does  not  occur  in  an  infil- 
trated apex,  but  this  change,  which  is  due  to  full  inflation  of  the 
lungs,  is  constant  in  health  and  in  atelectasis  of  the  apex.  The 
practical  utility  of  these  findings,  which  may  anticipate  the  other 
physical  signs,  is  obvious,  provided  that  they  are  correctly  inter- 
preted. Failure  to  obtain  an  x-ray  shadow  from  an  incipient  lesion 
that  affords  clear  physical  signs  occasionally  is  met  with  in  recent 
infiltrations  of  very  slight  density. 

At  a  later  period  of  the  disease,  when  the  tuberculous  foci  are  denser 
and  more  wide-spread,  their  shadows  are  correspondingly  deeper  and 


228 


PHYSICAL   DIAGNOSIS 


more  clear-cut,  oftentimes  because  of  their  contrast  with  the  excep- 
tional clearness  of  the  neighboring  emphysematous  pulmonary  tissue. 
A  large  cavity,  if  empty,  produces  a  pale  area,  with  peripheral  darken- 
ing; if  filled  with  fluid,  it  casts  a  definite  homogeneous  shadow. 
R6ntgen-ray  examination  does  not  reveal  the  presence  of  a  small 
cavity  in  the  midst  of  an  area  of  fibrosis.  The  accompanying  radio- 
graphs (Figs.  104, 105,  and  106)  serve  to  illustrate  the  shadows  cast 
by  various  degrees  of  tuberculous  infiltration. 
Palpation. — In  early  phthisis  deficiencies  of  expansion  so  slight 


Fig.  105. — Radiograph  of  phthisis  (cf.  Fig.  70).  Advanced  stage,  showing  dense 
consolidation  of  right  apex,  with  disseminated  infiltration  and  fibrosis  of  both  lungs. 
(Plate  by  Dr.  W.  F.  Manges.) 

as  to  escape  the  eye  are  frequently  appreciable  by  palpation,  and  this 
is  true  particularly  of  apical  lagging,  which  is  most  readily  detected 
by  palpating  the  clavicular  regions  from  behind,  as  elsewhere 
described.  (See  Fig.  75). 

Vocal  fremitus  is  exaggerated  over  infiltrated  areas  not  too  deep 
seated,  nor  too  effectually  covered  by  emphysema,  atelectasis,  or 
thickened  pleura.  In  view  of  the  relative  increase  of  vocal  fremitus 
at  the  right  apex,  it  follows  that  equal  intensity  of  the  fremitus  at 
both  apices  denotes  either  undue  increase  on  the  left  side  or  ab- 
normal decrease  on  the  right.  Other  conditions  being  the  same, 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         22Q 

the  more  compact  the  infiltration,  the  better  its  conduction  of  the 
voice  vibrations.  Over  an  empty  superficial  cavity  vocal  fremitus 
is  greatly  magnified,  but  over  one  filled  with  liquid  or  having  a 
plugged  bronchial  outlet  the  vibrations  are  entirely  abolished. 
It  is  occasionally  possible  to  feel  succussion  waves  over  a  large, 
smooth-walled  excavation  containing  thin  fluid  secretion. 

Mensuration  and  cyrtometry  of  the  chest,  save  as  a  means  of 
recording  striking  deformities,  are  generally  dispensed  with  in  the 
examinatioa  of  a  phthisical  thorax,  which  in  the  advanced  stages 
of  the  disease  shows  subnormal  expansion,  unusual  measurements 
of  the.  semicircumferences,  and  deviations  from  the  normal  depth 
and  breadth. 


Fig.  106. — Radiograph  of  phthisis  (cf.  Fig.  70).  Far-advanced  stage,  showing 
dense  infiltration  of  both  lungs,  especially  at  the  apices.  (Plate  by  Dr.  W.  F. 

Manges.) 

In  many  instances  unilateral  enlargement  of  the  axillary  and  super- 
ficial cervical  glands  on  the  side  of  an  apical  lesion  may  be  detected 
long  before  it  becomes  active.  These  glands,  which  Fernet  believes 
to  be  affected  secondarily  to  the  pulmonary  process,  are  small,  mov- 
able, painless,  and,  strangely  enough,  tend  to  disappear  as  the  primary 
infiltration  of  the  apex  lights  up.  Occasionally  the  subcutaneous 
lymphatic  glands  of  the  fourth  and  fifth  interspaces  in  the  axillary 
regions  are  distinctly  palpable.  Quite  different  from  such  indolent 


230  PHYSICAL    DIAGNOSIS 

adenopathies  are  the  soft,  ulcerative  forms  of  tuberculous  adenitis 
which  may  serve  as  the  determining  factor  of  phthisis. 

Percussion. — The  clavicular,  supraspinous,  and  interscapular 
regions  should  be  examined  for  the  earliest  indications  of  impaired 
resonance,  which  consist  of  a  percussion  sound  of  unduly  high  pitch 
and  brief  duration,  associated  with  a  sense  of  increased  resistance 
over  the  part  percussed.  These  evidences  of  moderate  infiltration 
are  gradually  accentuated  as  the  consolidation  increases  in  density 
and  in  extent,  until  finally  the  sound  becomes  frankly  dull  and  the 
resistance  extreme.  But  every  phthisical  lung  does  not,  during  its 
incipient  period,  alter  the  percussion  sound  in  this  manner,  for 
normal  resonance,  is  not  incompatible  with  a  deep-seated  compact 
infiltration,  of  considerable  size  entirely  surrounded  by  healthy 
lung,  nor  with  a  superficial  area  of  disseminated  foci.  The  presence 
of  an  apical  emphysema  also  is  to  be  recalled  as  a  potential  factor 
of  negativing  the  dulness  of  a  consolidation  in  this  region.  In 
attempting  to  judge  trifling  apical  differences  it  is  important  to 
draw  conclusions  after  comparative  percussion  of  the  two  sides, 
and  sometimes  impaired  resonance  of  one  apex  is  elicited  only  by 
fespiratory  percussion,  while  the  subject  holds  the  breath  after  a 
full  inspiration. 

Apart  from  the  demonstration  of  actual  dulness  at  the  apices,  the 
attempt  should  be  made  to  map  out  the  respiratory  rise  of  the  lungs  in 
these  regions,  by  percussion  over  the  supraclavicular  regions  from  be- 
hind. (See  Fig.  80,  p.  138.)  The  roughly  triangular  area  of  pulmonary 
resonance,  which  normally  extends  £  to  ij  inches  (1.25  103.75  cm-) 
above  each  clavicle  (Philip),  is  more  or  less  contracted  by  the  lung 
shrinkage  due  to  apical  disease.  Especially  significant  of  incipient 
phthisis,  according  to  Minor,  is  a  retraction,  or  outward  dislocation, 
of  the  inner  border  of  the  apex,  which,  in  health,  runs  upward  from 
the  sternoclavicular  joint  to  a  point  if  inches  (4  cm.)  internal  to  the 
free  edge  of  the  trapezius,  and  thence  drops  obliquely  to  the  lower 
border  of  the  second  thoracic  vertebra.  Extraordinary  skill  in  per- 
cussion is  obviously  necessary  to  detect  this  slight  apical  deviation. 

As  the  tuberculosis  spreads  through  the  lungs,  the  dulness  corre- 
spondingly extends,  acquiring,  over  areas  of  dense  fibrosis  and  pleural 
thickening,  a  characteristic  wooden  quality  quite  different  from  the 
dulness  of  airless  lung.  In  contrast  to  this,  a  decided  hyperresonance 
may  be  found  over  a  caseous  infiltration  undergoing  rapid  softening. 

A  cavity  affords  either  tympany  or  flatness,  depending  upon  whether 
it  be  empty  or  filled  with  fluid.  (See  Fig.  83.)  The  "cracked- 
pot  sound"  and  the  amphoric  "jug-sound"  are  also  to  be  sought  for, 
as  well  as  the  several  special  tonal  changes  described  by  Wintrich, 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        231 

Williams,  Friedreich,  and  Gerhardt.  (See  p.  148)  et  seq.)  In 
Landis's  experience  at  the  Phipps  Institute,  cavity  tympany  is 
elicited  in  about  70  per  cent,  of  cases  in  which  excavation  exists. 
It  is  sometimes  possible  to  empty  an  apical  cavity  by  gently  rapping 
upon  the  overlying  chest-wall  with  a  hard  instrument,  such  as  an 
ivory  paper-knife,  the  effect  being  to  excite  a  coughing  fit  which  expels 
the  secretion  within  the  cavity  and  thereby  develops  cavernous  signs — 
Erni's  signe  du  tapotage. 

In  most  cases  of  phthisis — and  also  in  numerous  other  diseases — 
sharp  immediate  percussion  of  the  upper  anterior  chest  causes  a  pe- 
culiar muscular  contraction,  known  as  myoidema,  appearing  either 
as  a  hard,  nodular  swelling  at  right  angles  to  the  course  of  the  muscle, 
or  as  a  linear  groove  running  in  the  direction  of  the  muscular  fibers. 

Auscultation. — Over  a  patch  of 'beginning  infiltration  the  inspiratory 
murmur  may  be  either  feeble  and  distant  or  loud  and  harsh,  the  former 
indicating  imperfect  entrance  of  air  into  the  tuberculous  area,  and 
the  latter,  consolidation  dense  enough  to  conduct  some  of  the  bron- 
chial tone.  The  expiratory  murmur  is  relatively  rough,  harsh,  and 
prolonged.  In  incipient  phthisis  of  the  right  apex  J.  S.  Billings,  Jr., 
finds  that  exaggerated  respiratory  and  voice  sounds  are  sharply 
restricted  to  the  apex,  while  a  similar  intensification  from  physiologic 
causes  is  audible  over  the  entire  upper  lobe. 

As  the  infiltration  extends,  the  respiration  becomes  bronchovesicular, 
and  finally  bronchial,  as  the  last  vestige  of  the  vesicular  element  is 
replaced  by  a  tubular,  blowing  quality.  Laennec's  "veiled  puff," 
recognized  as  an  abrupt  bronchial  tone  toward  the  end  of  an  inspira- 
tion beginning  as  a  vesicular  sound,  is  a  somewhat  distinctive  early 
sign;  and  respiration  of  the  interrupted  or  "cog-wheel"  type  is  quite 
common,  though  by  no  means  pathognomonic  of  phthisis.  Over 
parts  of  the  lung  affected  by  compensatory  distention,  exaggerated 
breathing  is  distinguishable. 

Over  a  cavity  of  fair  size  several  modifications  of  bronchial  breath- 
ing are  audible,  of  which  the  hollow  cavernous  and  the  echoing 
amphoric  types  are  the  most  distinctive;  over  a  small  cavity  the  breath- 
ing is  more  likely  to  be  purely  tubular.  Seitz-metamorphosing  res- 
piration, a  tubulocavernous  sound,  usually  inspiratory,  is  a  less  easily 
appreciable  sign,  occasionally  heard  over  a  cavity  with  a  small  bron- 
chial outlet. 

Vocal  resonance  is  increased  over  infiltrated  and  excavated  areas 
of  the  lung,  and  of  the  latter,  whispering  pectoriloquy  is  one  of  the 
most  constant  physical  signs;  it  may,  however,  also  be  symptomatic 
of  a  dense  peribronchial  solidification.  Clear  pectoriloquy  is  very 


232  PHYSICAL   DIAGNOSIS 

commonly  heard  in  this  condition  when  the  stethoscope  is  applied 
to  the  tips  of  the  upper  thoracic  vertebrae  (see  p.  301). 

Fine  moist  rales,  pleural  friction,  and  cavernous  bubbling  are  the 
most  pertinent  adventitious  sounds  of  chronic  ulcerative  phthisis. 
At  an  early  stage  moist  bronchiolar  subcrepitations,  still  finer  vesicular 
crepitations,  and  delicate  pleural  friction-sounds  are  to  be  expected; 
or,  should  the  bronchiolar  mucosa  be  dry  and  swollen,  piping  sibilant 
rales  are  found  rather  than  moist  sounds,  though  the  two  are  often 
intermingled.  In  some  instances  a  single  sharp  mucous  click  is 
the  first  evidence  of  the  tuberculous  bronchiolitis.  The  foregoing 
rales  are  chiefly,  if  not  altogether,  inspiratory,  and  are  usually  much 
influenced  by  coughing  and  by  deep  breathing;  their  persistence  at 
an  apex  is  one  of  the  earliest,  most  convincing  indications  of  tuber- 
culosis in  this  region.  Boeri  advises  auscultation  immediately  after 
active  massage  of  the  supraclavicular  regions,  as  a  means  of  identi- 
fying delicate  apical  crepitations  otherwise  inaudible;  or  they  may 
be  developed  by  instructing  the  patient  to  cough  lightly  at  the 
end  of  expiration. 

If  an  area  of  pulmonary  infiltration  near  the  heart  be  forcibly 
jogged  by  the  cardiac  impact,  audible  vibrations  may  be  set  up  in 
the  exudate  within  the  bronchioles  and  infundibula  of  the  diseased 
area,  thus  producing  so-called  cardiac  or  cardiopneumatic  rales. 
By  a  similar  mechanism  air  may  be  driven  from  the  finer  tubes 
with  an  audible  systolic  whiff,  known  as  a  cardiorespiratory  murmur. 

Pleural  friction,  which  is  generally  demonstrable  throughout  the 
disease,  may  be  restricted  to  the  pleural  layers  overlying  the  heart, 
in  consequence  of  which  the  sound  conforms  to  the  rhythm  of  pleuro- 
pericardial  friction  (q.  v.).  Pleural  thickening,  it  is  to  be  remem- 
bered, may  be  so  extensive  as  to  mask  exaggerated  fremitus,  as  well 
as  to  dull  the  percussion  sound  over  an  otherwise  tympanitic  area. 
Vascular  murmurs,  due  to  the  pressure  of  a  thickened  pleura,  are 
occasionally  demonstrable  over  the  subclavian  arteries  in  tuber- 
culosis of  the  apex. 

As  softening  progresses  and  secretion  accumulates  within  the 
larger  bronchi,  coarse  mucous  rales  become  audible,  and,  should  dry 
bronchitis  coexist  in  other  parts  of  the  tubes,  snoring  rhonchi  are  also 
heard. 

Over  a  cavity  containing  liquid  there  are  various  sized  moist  bub- 
bling and  gurgling  sounds  of  cavernous  or  amphoric  quality,  but  a  dry 
cavity  affords  no  such  physical  signs.  To  cavernous  rales,  deep  and 
active  inspiration  may  add  a  sharp,  clean-cut  quality,  described  by 
Skoda  as  consonating  or  resonant,  and  metallic  rales  thus  modified 
bear  some  resemblance  to  the  metallic  tinkle  of  hydrothorax,  from 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         233 

which,  however,  they  are  readily  distinguished  by  the  associated 
physical  signs.  Exceptionally,  a  cavity  of  large  size  furnishes  a 
succussion  sound  similar  to  the  pleural  splash.  Cavernous  rales 
may  also  be  of  the  cardiopneumatic  type,  in  case  an  area  of  con- 
solidation riddled  with  small  cavities  happens  to  be  bound  down  to 
the  heart  by  dense  pleural  adhesions.  (See  p.  166.)  The  trans- 
mitted- sounds  of  the  heart,  and  frequently  of  murmurs,  should  they 
exist,  are  clearly  heard  over  large  apical  cavities. 

Under  the  term  laryngeal  crepitus  Remouchamps  describes  a  fine 
grating  respiratory  sound,  detected,  even  in  incipient  phthisis,  by 
placing  the  ear  a  few  inches  from  the  open  mouth  of  the  subject, 
who  meanwhile  breathes  deeply,  with  the  chin  elevated  and  ex- 
tended. By  this  manceuver  a  bruit,  comparable  to  the  scratching 
of  a  pen  upon  a  rough  surface,  is  audible  during  respiration,  espe- 
cially with  expiration.  The  sound  is  due  presumably  to  the  laryn- 
geal amplification  of  adventitious  sounds  arising  in  the  diseased 
tissues  of  the  lung. 

Diagnosis. — No  sign,  however  trivial  it  appears,  should  be  dis- 
regarded in  the  study  of  a  case  of  possible  incipient  phthisis,  for  the 
diagnosis  of  which  pulmonary  physical  signs  alone  may  be  wholly 
inadequate.  Advanced  cases,  on  the  contrary,  present  no  such  diffi- 
culty, but  a  tuberculous  lesion  whose  inroads  afford  convincing 
physical  signs  is  correspondingly  hard  to  arrest,  and  in  such  an  event 
the  physician  may  be  able  to  do  little  save  advise  the  patient  to  put 
his  house  in  order  against  the  inevitable  finality. 

In  some  instances  a  beginning  infiltration  is  betrayed  by  deficient 
expansion,  exaggerated  voice  fremitus  and  resonance,  a  high-pitched 
percussion  sound,  an  impure  respiratory  murmur,  and  a  few  fine 
moist  rales  over  a  circumscribed  area,  generally  at  an  apex.  In 
others  there  is  merely  an  enfeebled  or  a  harsh  respiratory  sound, 
with  perhaps  an  occasional  mucous  click  or  a  few  subcrepitations. 
For  the  patient's  sake,  it  is  better  to  regard  as  tuberculous  these 
evidences  of  a  local  bronchiolitis,  if  they  persist  at  an  apex,  despite 
negative  sputum  examinations  and  an  unaltered  percussion  sound,  and 
in  doubtful  cases  of  this  sort  tuberculin  may  clear  up  the  diagnosis 
at  once.  Aside  from  the  local  physical  signs,  it  is  essential  to  take 
into  account  many  other  evidences  of  the  more  or  less  active  inroads 
of  the  tuberculous  process — habitually  rapid  pulse,  afternoon  fever 
and  shivering,  spontaneous  sweating,  indolent  adenitis,  cough  and 
huskiness  of  the  voice,  persistent  nasopharyngeal  catarrh,  capricious 
appetite  and  chronic  indigestion,  slight  secondary  anemia,  and  pro- 
gressive languor  and  loss  of  weight.  Very  commonly  the  chief  symp- 
toms are  those  of  chronic  bronchitis  or  of  pleurisy,  while  sometimes 


234  PHYSICAL   DIAGNOSIS 

hemoptysis  is  the  first  evidence  found.  Some  patients  exhibit  an 
extraordinary  degree  of  tolerance  to  the  constitutional  effects  of  the 
tuberculotoxin,  and  are  not  conscious  of  any  decided  ill  health  until 
the  lungs  have  become  extensively  damaged;  and  in  others  the  pul- 
monary lesions  are  overshadowed  by  symptoms  relating  to  tuber- 
culosis of  other  parts  of  the  body. 

Malarial  fever  may  be  simulated  by  phthisical  attacks  of  chills, 
fever,  and  sweats,  closely  conforming  to  the  paroxysms  of  ague,  but 
the  chest  signs,  the  result  of  the  blood  and  sputum  examinations,  and 
the  patient's  history  furnish  conclusive  data  for  differentiating  the 
two  infections. 

Chronic  bronchitis  must  be  carefully  distinguished  from  those 
forms  of  pulmonary  tuberculosis  having  marked  signs  of  bronchial 
implication.  In  ordinary  chronic  bronchial  catarrh  it  is  common 
to  find  the  chest  more  or  less  emphysematous,  with  general  hy- 
perresonance,  diminished  fremitus,  feeble  breath-sounds,  greatly 
prolonged  expiration,  and  numerous  dry  and  moist  bronchial  rales 
of  various  size. 

The  discrimination  between  bronchiectasis  and  a  tuberculous  cavity 
is  always  difficult  and  frequently  impossible.  Basal  cavity  signs 
that  persist  without  becoming  exaggerated,  paroxysms  of  coughing 
productive  of  fetid  sputum  containing  no  tubercle  bacilli,  absence  of 
apical  infiltration,  and  little  or  no  disturbance  of  the  patient's  strength 
and  nutrition  are  findings  in  favor  of  a  non-tuberculous  bronchial 
dilatation.  The  bronchiectatic  "evacuative  cough,"  which  empties 
the  cavity,  must  be  distinguished  from  the  phthisical  "Morton's 
cough,"  which  empties  the  stomach,  often  so  repeatedly  and  effect- 
ually that  the  patient's  nutrition  suffers. 

A  careful  examination  of  the  lungs  is  sufficient  to  identify  cases  of 
tuberculosis  which  masquerade  as  chlorosis,  secondary  anemia,  and 
chronic  gastric  catarrh.  Phthisis  versus  pulmonary  abscess  and 
gangrene  is  discussed  elsewhere.  (See  p.  255  et  seq.) 

FIBROID   PHTHISIS   (Tuberculofibrosis    or   Fibrotuberculosis   of    the 

Lungs) 

Clinical  Pathology. — The  predominant  lesion  in  this  variety  of 
phthisis  consists  of  a  dense  fibrous  overgrowth  whereby  the  tubercu- 
lous areas  are  compressed,  encapsulated,  and  finally  segregated  or 
obliterated.  The  affection  is  one  of  decided  chronicity,  and  develops 
apparently  in  subjects  of  great  vital  resistance,  infected  with  tubercle 
bacilli  of  moderate  virulence,  owing  to  which  conditions  this  con- 
servative cirrhosis  destroys  the  tuberculous  foci,  limits  their  dissemi- 
nation, and  in  some  instances  effectually  arrests  the  progress  of  the 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        235 

initial  phthisical  disease.  In  lungs  cirrhosed  in  this  manner  the 
original  tubercles  are  entirely  effaced,  or  else  are  recognizablfe  merely 
as  encapsulated  areas  of  sclerosis  and  as  partly  obliterated  excava- 
tions. The  latter,  as  in  ulcerative  phthisis,  occasionally  are  of  con- 
siderable size,  and  contain  infective  material  which,  in  the  course  of 
time,  may  break  through  the  cavity  wall  and  contaminate  the  sur- 
rounding structures.  Other  cavities,  of  smaller  size,  may  be  com- 
pressed into  long,  slender  fistulous  passages  drained  by  neighboring 
bronchial  tubes — the  cicatrices  fistuleuses  of  Laennec. 

Ultimately,  the  fibroid  changes,  although  primarily  reparative  in 
character,  become  so  exaggerated  as  seriously  to  interfere  with  the 
pulmonary  function,  for  they  progressively  encroach  upon  the  alve- 
olar tissue,  thus  decreasing  the  respiratory  area  and  exciting  com- 
pensatory dilatation  of  the  non-fibroid  vesicles,  and  in  time  produce 
an  extreme  degree  of  induration  and  contraction  of  the  pulmonary 
structure.  In  the  event  of  extensive  pleuropulmonary  adhesion  and 
contraction,  conspicuous  deformity  of  the  thoracic  wall  develops. 

Fibroid  phthisis  is  ordinarily  a  sequel  of  the  chronic  ulcerative 
type  of  the  disease  or  of  a  tuberculous  pleurisy,  but  it  maybe  secondary 
to  other  forms  of  tuberculosis  of  the  lungs;  or  there  may  be  a  primary 
fibrosis,  subsequently  becoming  tuberculous.  The  process  usually 
implicates  both  lungs,  and  tends  to  become  most  extensive  at  one  of 
the  apices.  Few  sufferers  from  fibroid  phthisis  escape  bronchiecta- 
sis,  mainly  because  of  the  frequent  incidence  of  dense  fibrous 
adhesions  which  exert  traction  upon  the  bronchial  walls.  In  con- 
sequence of  the  habitual  obstruction  to  the  pulmonary  circulation 
that  exists,  cardiac  hypertrophy,  particularly  of  the  right  ventricle, 
sooner  or  later  supervenes. 

Physical  Signs. — Inspection. — The  pulmonary  contraction  inevit- 
ably changes  the  contour  of  the  thorax,  drags  the  heart  from  its  normal 
site,  and  disturbs  the  respiratory  excursions,  especially  where  the 
fibrosis  is  wide-spread  and  complicated  by  extensive  pleural  thicken- 
ing and  by  bronchiectasis.  On  the  affected  side,  the  respiratory 
movements  are  restricted,  perhaps  to  the  point  of  practical  oblitera- 
tion, while  the  opposite  half  of  the  chest,  provided  that  it  has  escaped 
extensive  fibrosis,  is  vicariously  enlarged.  The  thoracic  wall  is 
flat  and  depressed,  either  as  a  whole  or  locally;  the  shoulder  droops; 
the  clavicular  areas  are  unduly  deep;  the  interspaces  are  narrowed 
or  even  effaced  by  the  crowding  together  and  overlapping  of  the  ribs; 
and  the  diaphragm  is  elevated  above  its  normal  level.  In  the  extreme 
instance  the  spinal  column  inclines  toward  the  shrunken  side.  The 
heart  is  usually  drawn  toward  the  affected  area,  the  apex -beat  being 
displaced  toward  the  right  axilla  by  fibrosis  of  the  right  lung,  and 


236 


PHYSICAL   DIAGNOSIS 


toward  the  left  axilla  by  a  left-sided  lesion ;  in  the  latter  the  im- 
pulse of  the  heart  is  frequently  visible  upon  the  chest -wall  from 
the  second  to  the- fifth  interspaces.  Owing  to  the  enlargement  of 
the  right  heart  there  are  bulging  of  the  lower  part  of  the  sternum 


I 


Fig.  107. — Radiograph  of  fibroid  phthisis.     Extensive  fibrosis  of  left  lung,  with  corre- 
sponding cardiac  displacement.     (Plate  by  Dr.  W.  Manges.) 

and  pulsation  in  the  epigastrium  and.  in  the  upper  interspaces  to 
the  right  of  the  sternum. 

Palpation. — The  intensity  of  the  local  fremitis  varies  according 
to  the  character  of  the  associated  pulmonary  and  pleural  lesions. 
Although  the  voice-sounds  are  clearly  conducted  by  cirrhotic  lung 
tissue,  they  are  often  diminished  in  fibroid  phthisis,  owing  to  the 
influence  of  pleural  thickening,  emphysema,  bronchial  obstruc- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         237 

tion,  and  retraction  of  the  lung  from  the  chest-wall.  Over  apical 
cirrhosis  there  is  usually  exaggeration  of  the  fremitus,  but  over  a 
central  lesion  no  such  alteration  is  appreciable. 

Percussion. — Wooden  dulness  and  a  sense  of  extreme  resistance 
to  the  pleximeter  finger  are  elicited  over  the  fibroid  areas,  especially 
when  there  are  great  pleural  thickening  and  costal  overlapping. 
Hyperresonance  is  the  rule  on  the  emphysematous  side,  as  well  as 
over  circumscribed  patches  of  overdistended  lung  adjacent  to  the 
seats  of  fibrosis.  Circumscribed  hyperresonance  or  pure  tympany 
at  the  base  of  the  lungs  suggests  an  empty  bronchial  dilatation, 
and,  at  the  apex,  a  pulmonary  cavity. 

Auscultation. — Various  degrees  of  bronchophony  and  bronchial 
breathing  are  audible,  ranging  from  the  slightly  increased  vocal 
resonance  and  bronchovesicular  breathing  of  a  partly  cirrhosed  area, 
to  the  clear  pectoriloquy  and  bronchial  or  amphoric  breathing  of 
a  compact  fibrosis  or  of  a  cavity.  Such  changes  are  likely  to  be 
more  marked  at  the  apices  than  at  the  bases,  where  feeble  respiration 
and  many  moist  rales  are  ordinarily  found.  Other  rales  are  also 
to  be  looked  for,  owing  to  the  common  association  of  bronchitis, 
tuberculous  softening,  and  pleurisy.  As  the  right  heart  dilates,  the 
murmur  of  tricuspid  incompetency  appears,  and  the  pulmonic  second 
sound,  previously  accentuated  and  ringing,  gradually  weakens. 

Diagnosis. — With  a  deformed  chest,  cardiac  displacement  and 
right-sided  enlargement,  wooden  dulness,  intensified  respiratory 
and  voice-sounds,  and  signs  of  pulmonary  softening  or  excavation, 
the  diagnosis  is  generally  clear.  With  nothing  more  than  physical 
signs  of  fibrosis  as  a  guide,  the  question  of  fibroid  tuberculosis  versus 
non-tuberculous  interstitial  pneumonia  arises,  and  in  making  this 
distinction  one  is  frequently  forced  to  depend  finally  upon  the  results 
of  sputum  examination  and  the  tuberculin  reaction.  The  detection 
of  bilateral  lesions,  together  with  the  fact  that  the  patient  has  or  has 
had  fever,  sweats,  loss  of  weight,  and  other  suspicious  systemic  symp- 
toms, are  suggestive  of  the  tuberculous  character  of  the  process. 

PULMONARY    SYPHILIS    (Syphilitic  Pneumonia  or  Fibrosis;  "White 
Pneumonia;  White  Hepatization  of  the  Lung;  Pulmonary  Albinism) 

Clinical  Pathology. — Pulmonary  syphilis  deserves  careful  con- 
sideration, not  on  account  of  its  common  incidence,  for  it  is  rare, 
nor  because  of  its  distinctive  physical  signs,  for  there  are  none,  but 
rather  because  of  its  close  clinical  resemblance  to  certain  non-syphilitic 
affections  of  the  bronchopulmonary  system,  from  which  the  differen- 
tiation of  true  lues  of  the  lung  must  be  attempted. 


238  PHYSICAL  DIAGNOSIS 

Gummata,  interstitial  fibrosis,  and  white  hepatization  of  the 
vesicular  structures  are  the  essential  pathologic  changes  of  this  rarely 
diagnosed  condition,  of  which  two  sharply  denned  types,  the  acquired 
and  the  congenital,  are  generally  recognized.  In  acquired  syphilis 
of  the  lung  the  lesions  are  of  gummatous  and  fibroid  character,  the 
former,  though  very  rare,  being  by  far  the  more  distinctive  of  the  two. 
Although  they  may  invade  any  part  of  the  lung,  gummata  are  most 
often  situated  toward  the  root,  near  the  larger  bronchi,  or,  indeed, 
these  tubes  may  be  directly  implicated  by  the  granulomata,  and  in 
consequence  are  likely  to  become  the  seat  of  stenosis  and  of  traction 
diverticula.  Ordinarily,  a  gumma  does  not  exceed  3  or  4  inches 
(7.5  to  10  cm.)  in  greatest  diameter,  and  consists  of  a  gray  or  yellowish 
caseous  mass,  inclosed  by  a  fibrous  capsule,  either  resilient  and  trans- 
lucent or  rigid  and  dense,  according  to  the  age  of  the  lesion.  Necrosis 
and  liquefaction  of  a  gumma,  with  its  rupture  into  a  bronchus,  leads 
to  cavity  formation,  and  absorption  and  cicatrization  of  the  syphilitic 
focus  results  in  scarring  at  its  site.  Interstitial  fibrosis  is  sometimes 
associated,  and,  exceptionally,  it  appears  to  develop  as  a  primarily 
leutic  process,  quite  independent  of  gummatous  growths.  As  a  rule, 
the  fibrosis  begins  at  the  root  of  the  lung,  and  extends  peripherally 
along  the  interlobular  and  interlobar  septa,  but  occasionally  it  spreads 
in  the  reverse  direction,  being  of  pleurogenous  origin.  The  con- 
dition is  virtually  a  chronic  interstitial  pneumonia  (q.  v.),  commonly 
of  a  lobar  type,  and  attended  by  the  pathologic  changes  in  the  vesic- 
ular structures,  bronchi,  and  pleura  incident  to  an  ordinary  cirrhosis 
of  the  lung.  Acquired  pulmonary  syphilis  may  lack  distinctive 
features,  for  a  gumma  may  exactly  resemble  a  caseous  tuberculous 
mass,  and  a  syphilitic  cirrhosis  does  not  differ  from  cirrhoses  due  to 
other  factors.  In  the  first  instance  the  differentiation  depends  upon 
the  presence  of  the  tubercle  bacillus,  the  syphilitic  treponema  almost 
never  being  found  in  a  gumma;  while  in  the  second  instance  the 
most  available  differential  criteria  are  the  patient's  history  and  the 
question  of  cutaneous  scars  and  visceral  lesions.  Congenital  syphilis 
of  the  lung  is  typified  by  a  condition  known  as  white  pneumonia  oj 
the  fetus,  characterized  by  hyperplasia  of  the  intervesicular  walls 
and  proliferation  of  the  cells  lining  the  vesicles,  with  consequent 
obliteration  of  the  vesicular  structure  through  various  areas,  scattered 
or  diffuse,  of  the  lung  or  lungs.  The  affected  parts  teem  with  Trepo- 
nema pallida,  and,  owing  to  the  hyperplasia,  become  anemic,  airless, 
and  consolidated,  being  distinguishable  as  firm,  non-crepitant, 
grayish-white  territories,  described  as  white  hepatization  of  the  lung. 
White  pneumonia  is  found  in  the  fetus,  in  still-born  infants,  and 
in  those  born  alive,  but  in  the  last  named  no  stress  of  respiratory 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        239 

effort,  however  strong,  is  sufficient  to  inflate  the  consolidated 
areas.  Gumma  affects  the  congenitally  syphilitic  lung  but  very 
rarely. 

Physical  Signs  and  Diagnosis. — That  acquired  syphilis  of  the 
lung  is  attended  by  no  distinctive  thoracic  signs  must  be  apparent 
when  the  nature  of  the  several  pulmonary  lesions  is  considered. 
According  to  the  conditions  predominating  in  the  individual  case, 
the  physical  signs  ordinarily  suggest  chronic  ulcerative  phthisis, 
bronchostenosis,  bronchiectasis,  or  pulmonary  fibrosis. 

Phthisis  is  counterfeited,  not  alone  by  signs  of  consolidation  and 
perhaps  of  excavation,  but  also  by  the  occurrence,  with  greater  or 
less  constancy,  of  cough,  dyspnea,  mucopurulent  and  bloody  sputum, 
pleural  pain,  night-sweats,  and  emaciation.  These  last  three  symp- 
toms are,  however,  comparatively  infrequent,  and,  when  present, 
are  usually  not  striking — a  circumstance  of  some  consequence  in 
favor  of  lues.  But  of  far  greater  suggestiveness  is  the  fact  that  the 
sputum  invariably  remains  free  from  tubercle  bacilli,  in  spite  of  its 
apparently  tuberculous  appearance  and  notwithstanding,  in  many 
instances,  the  clinical  evidences  of  advanced  consumption.  Appar- 
ently, true  syphilis  organisms  are  never  found  in  the  sputum,  judging 
from  Rosenberger's  analysis  of  1210  collected  cases.  The  reputed 
tendency  of  syphilis  primarily  to  affect  the  middle  lobe  of  the  right 
lung,  and  the  predilection  of  the  right  apex  for  tuberculous  infection, 
are  of  minor,  but  not  wholly  negligible,  significance.  If  the  patient 
in  past  years  has  sown  the  wind  so  as  now  to  reap  a  luetic  whirlwind, 
syphilis,  rather  than  tuberculosis  of  the  lungs,  is  strongly  suggested, 
this  inference  becoming  the  stronger  if  it  be  possible  to  identify  the 
scar  of  the  initial  lesion,  and  to  find  signs  of  arteriosclerosis  and  of 
syphilitic  processes  elsewhere.  Finally,  so  far  as  phthisis  is  concerned, 
the  diagnosis  may  be  settled  by  the  tuberculin  test:  if  positive,  the 
lesion  is  tuberculous,  though,  unfortunately,  this  does  not  necessarily 
rule  out  coexisting  syphilis  of  the  lung;  but  a  negative  reaction  with 
tuberculin  excludes  phthisis,  and  by  the  same  token  indicates  syph- 
ilis— beyond  all  question  if  it  be  associated  with  a  strongly  positive 
Wassermann  reaction.  If  tempted  to  use  potassium  iodid  as  a 
therapeutic  test,  one  should  weigh  the  baneful  effects  of  this  drug 
in  lighting  up  a  tuberculous  process  against  its  action  in  subduing 
lues.  Much  the  better  plan  is  to  anticipate  improvement  under 
the  use  of  salvarsan. 

Bronchial  stenosis,  due  to  the  encroachment  of  gummatous  nodules 
or  to  stricture  by  scar  tissue,  must  be  distinguished  from  bronchial 
occlusion  by  aneurism  and  by  malignant  tumor,  especially  sarcoma. 
Aneurismal  pressure  generally  can  be  definitely  proved  with  the  aid, 


240  PHYSICAL    DIAGNOSIS 

of  the  x-ray,  even  if  the  classic  physical  signs  of  this  lesion  be  lacking. 
(See  Aneurism,  Section  VI.)  A  history  of  syphilis  and  the  existence  of 
arteriosclerosis,  it  should  be  noted,  favor  aneurism  as  well  as  gumma. 
The  following  points  are  in  favor  of  sarcoma  rather  than  gumma :  signs 
of  consolidation  in  the  anterior  mediastinum  prior  to  the  onset  of  the 
bronchial  obstruction;  rapidly  developing  and  often  conspicuous 
symptoms,  referable  chiefly  to  the  mediastinal  vascular  trunks  and 
nerves;  initial  or  secondary  metastatic  growths  in  parts  remote  from 
the  thorax;  anemia  or  cachexia  of  the  patient,  a  clean  personal  history, 
and  no  scars  or  other  relics  of  syphilis;  and  an  unaltered  clinical 
picture,  despite  the  subject's  saturation  with  iodids  and  mercury. 
Here  also  the  x-ra.y  may  be  Of  service,  both  in  making  the  initial 
diagnosis  and  because  of  the  fact  that  sometimes  malignant  growths 
diminish  extraordinarily  under  persistent  rontgenization,  while  gum- 
mata  do  not. 

The  physical  signs  of  syphilitic  bronchiectasis  are  in  no  wise  dis- 
tinctive, so  that  its  differentiation  from  bronchial  dilatation  due  to 
other  causes  rests  upon  other  clinical  evidence.  The  same  is  true 
of  syphilitic  fibrosis  of  the  lung  and  its  attempted  discrimination 
from  other  types  of  chronic  interstitial  pneumonia. 

Congenital  syphilis  of  the  lung  is  usually  revealed  only  at  autopsy, 
inasmuch  as  it  is  prone  to  affect  still-born  infants  or  those  dying  soon 
after  birth.  Occasionally  white  pneumonia  is  suggested  by  finding 
consolidative  and  other  evidences  of  bronchopneumonia  in  a  young 
baby  showing  unmistakable  stigmata  of  congenital  syphilis. 

EMPHYSEMA 

The  word  emphysema,  literally  meaning  inflation,  is  applied,  with 
an  appropriate  adjective,  to  several  distinct,  but  frequently  inter- 
dependent, pulmonary  lesions  of  widely  diverse  character,  affecting 
the  vesicular  and  interstitial  structures,  either  singly  or  together. 
Of  the  veskular  type  of  emphysema  there  are,  according  to  current 
clinical  nomenclature,  four  varieties:  the  hypertrophic  or  large-lunged, 
or  a  condition  of  chronic  vesicular  dilatation  and  septal  wasting 
eventually  leading  to  increased  pulmonary  volume;  the  atrophic  or 
small-lunged,  characterized  by  extreme  and  progressive  atrophy 
of  the  vesicular  structures,  resulting  in  diminution  of  the  pulmonary 
volume;  the  acute  vesicular,  in  which  a  widely  diffused  overdistention 
of  the  lungs  suddenly  develops;  and  the  compensatory,  or  a  more  or 
less  circumscribed  overinflation  of  the  vesicles,  either  acute  or  chronic 
in  character,  and  not  primarily  attended  by  permanent  structural 
damage.  The  term  interstitial  emphysema  is  used  to  designate  an 
accumulation  of  air  in  the  interstitial  connective  tissues  of  the  lung. 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        241 


HYPERTROPHIC   EMPHYSEMA   (Large-lunged,  Pseudohypertrophic,  Sub- 
stantive, True,  or  Idiopathic  Emphysema ;  Alveolar  Ectasia) 

Clinical  Pathology. — In  this  type  of  emphysema  the  lungs  are 
permanently  overinflated  as  the  result  of  impaired  pulmonary  elastic- 
ity, combined  with  a  state  of  persistent  intravesicular  hypertension 
(Fig.  1 08).    The  use  of  the  adjectives  hypertrophic  and  pseudo- 
Large  bulla 


Emphysema  tous 
border  of  lung  i 


Large  bulla 
Fig.  108. — Pulmonary  emphysema  (Jefferson  Hospital  Laboratories). 

hypertrophic  to  denote  this  form  of  emphysema  relates  merely  to 
the  enlarged  volume  of  the  lungs,  and  not  to  the  predominant  tissue 
changes,  which  are  essentially  atrophic.  Impaired  pulmonary 
elasticity  may  be  an  hereditary  taint,  whereby  the  elastic  tissue  of  the 
lungs  is  inherently  deficient  or  subnormally  resistant;  or  the  defect 
may  be  acquired  through  damage  by  processes  inducing  degeneration 
and  atrophy  of  the  elastic  fibers,  such  as,  for  example,  chronic  bron- 
chial catarrh,  atheroma,  and  similar  factors  of  disordered  nutrition. 

16 


242  PHYSICAL   DIAGNOSIS 

Given  a  predisposition  of  this  sort,  increased  intravesicular  pres- 
sure, especially  when  due  to  expiratory  strain  or  overdistention, 
acts  as  the  determining  cause  of  emphysema.  Emphysema  is 
directly  related  to  impaired  alveolar  ventilation,  with  an  increase 
in  the  dead  space  of  the  lungs  due  chiefly  to  atonic  elongation  and 
broadening  of  the  bronchioles  and,  in  part,  to  bronchiolar  spasm 
(Hoover). 

Expiratory  overdistention  of  the  vesicles,  the  ruling  factor  in  most 
cases,  attends  violent  expiratory  efforts  associated  with  obstruction  to 
the  free  outlet  of  the  air-columns.  Thus,  in  paroxysms  of  coughing  the 
closure  of  the  glottis  plus  the  active  pressure  of  the  chest-wall  together 
provoke  inordinate  tension  within,  and  undue  stretching  of,  the  air-vesi- 
cles, especially  toward  the  apices  and  along  the  anterior  margins  of  the 
lungs,  where  the  pulmonary  structure,  being  poorly  supported  by  the 
parietes,  becomes  the  natural  target  of  the  violent  gusts  of  air  which, 
owing  to  the  closed  glottis,  cannot  escape  by  their  natural  channels. 
The  poor  support  afforded  by  the  intercostal  muscles  possibly  has 
something  to  do  with  the  development  of  emphysema  in  other  por- 
tions of  the  lungs,  which  are  successively  approximated  to  the  yielding 
interspaces  during  the  progressive  emphysematous  changes  in  costal 
contour.  Chronic  bronchitis,  asthma,  and  pertussis,  chiefly  in  that 
they  excite  extreme  intravesicular  tension  during  expiration,  are 
prominent  causes  of  emphysema.  In  the  light  of  modern  studies 
(by  Schmidt,  Prettin,  and  others)  the  old  belief  that  glass-blowers 
and  players  of  wind  instruments  are  peculiarly  prone  to  emphysema 
must  be  regarded  as  a  medical  tradition. 

Inspiratory  overdistention  of  the  vesicles  apparently  has  little,  if 
any,  bearing  upon  the  production  of  true  large-lunged  emphysema, 
though  it  is  a  most  potent  factor  of  the  so-called  compensatory 
variety  (q.  v.) .  It  is,  however,  conceivable  that  a  variable  degree  of 
vesicular  dilatation  might  arise  should  relatively  excessive  inspira- 
tory  movements  and  shallow,  imperfect  expiration  coexist,  as  is 
the  tendency  when  the  thoracic  resiliency  is  impaired  by  age  or  by 
disease. 

Postmortem,  the  distinguishing  marks  of  emphysematous  lungs 
are  their  immoderate  bulk,  diminished  weight,  pale  appearance, 
and  disinclination  to  collapse;  they  convey  a  peculiar  feathery  sen- 
sation when  handled,  and  their  borders  extend  far  beyond  the  normal 
limits,  conspicuously  encroaching  anteriorly  upon  the  cardiac  and 
the  hepatic  areas.  The  emphysematous  tissue  fails  to  crepitate, 
pits  easily  on  pressure,  and  is  recognized  beneath  the  pleura  as  a 
series  of  globular  or  irregular  bullae,  ranging  in  size  from  a  few  milli- 
meters to  several  centimeters,  and,  as  a  rule,  attaining  their  maximum 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        243 

development  along  the  anterior  inferior  margins,  at  the  root  of 
the  lower  lobes,  and  at  the  apices  of  the  lungs.  Fig.  108  shows 
the  appearance  of  these  large  emphysematous  air-bladders  along 
the  pulmonary  borders.  On  cross-section  of  a  dry  inflated  speci- 
men, the  lung  is  found  to  be  riddled  with  these  enlarged  vesiculo- 
infundubular  compartments,  both  single  and  multilocular,  formed 
by  the  rupture  and  coalescence  of  numerous  individual  over- 
distended  vesicles.  Microscopically,  the  changes  relate  to  atrophy, 
thinning,  and  perforation  of  the  intervesicular  walls,  obliteration 
of  the  capillary  network  therein,  quantitative  and  qualitative  deterio- 
ration of  the  elastica,  and  degeneration  of  the  alveolar  epithelium. 
Bronchitis  and  peribronchial  thickening  are  virtually  constant,  and 
ectases  of  the  finer  bronchi  are  frequent  associated  changes.  The 
pleura  is  generally  dry  and  pale,  and  may  show  the  white  patches 
of  Virchow's  "pulmonary  albinism."  The  rupture  into  the  pleural 
cavity  of  an  emphysematous  bulla  may  set  up  pneumothorax.  Owing 
to  the  stress  imposed  upon  it  by  the  impeded  pulmonary  circulation, 
the  right  side  of  the  heart  undergoes  hypertrophy  and  dilatation, 
and  occasionally  a  general  cardiac  enlargement  supervenes;  the  pul- 
monary artery  may  be  dilated  and  atheromatous.  Various  organs, 
notably  the  liver,  spleen,  and  kidneys,  show  the  familiar  structural 
changes  induced  by  chronic  venous  congestion. 

Physical  Signs. — Inspection. — The  permanently  overinflated 
"barrel  chest,"  described  in  a  preceding  section  (see  p.  78),  is  dis- 
tinctive of  advanced  cases  of  many  years'  development,  although  this 
deformity  is  by  no  means  invariable.  In  certain  subjects  the  costal 
cartilages  are  abnormally  thickened  and  lengthened,  corresponding  to 
the  "  specific  calcification  "  exploited  half  a  century  ago  by  Freund,  as 
a  primary  and  specific  emphysematous  change.  Dyspnea,  cough, 
cyanosis,  and  clubbing  of  the  finger-tips  are  important  objective  signs 
which  become  more  and  more  marked  as  the  disease  advances,  with 
consequent  loss  of  pulmonary  elasticity,  restriction  of  the  respiratory 
surface,  defective  blood  aeration,  and  exaggeration  of  the  bronchitic 
lesions.  When  the  right  heart  fails  under  the  stress  of  the  intrapul- 
monary  hypertension,  these  signs  become  most  striking,  and  are 
attended  by  jugular  pulsation,  general  venous  turgescence,  and  edema. 
Epigastric  pulsation,  due  to  the  movements  of  a  displaced  and 
enlarged  heart,  is  common,  but  the  true  apex-beat  is  obscured  by 
the  interposed  mass  of  emphysematous  lung.  During  respiration 
the  thorax  rises  and  falls  en  masse  in  a  vertical  direction,  but  fails 
to  expand  normally,  despite  the  strenuous  attempts  of  the  aux- 
iliary muscles  to  overcome  the  rigidity  of  the  chest-walls.  Litten's 
shadow  begins  at  a  lower  level  and  is  shorter  than  in  the  healthy 


244  PHYSICAL    DIAGNOSIS 

chest,  owing  to  the  abnormally  low  position  and  limited  mobility 
of  the  diaphragm.  In  the  exceptional  instance  this  muscle  is  so 
extremely  depressed  and  relaxed  that  its  convexity  lies  toward 
the  abdomen  instead  of  toward  the  thorax.  This  inverted  position 
of  the  diaphragm,  whereby  it  serves  as  an  expiratory  rather  than 
as  an  inspiratory  muscle,  gives  rise  to  what  is  termed  an  inverse 
type  of  respiration.  The  fossae  above  the  clavicles  and  sternum  and 
the  upper  intercostal  spaces  may  be  sucked  in  with  deep  inspiration, 
while  the  lower  interspaces  tend  to  become  obliterated,  or  even  to 
balloon  outward,  during  expiration.  Sudden  inflation  of  both  supra- 
clavicular  spaces  sometimes  accompanies  a  coughing  fit  severe  enough 
violently  to  distend  the  air-vesicles  of  the  apices. 

Palpation. — Bilateral  enfeeblement  of  vocal  fremitus  is  a  character- 
istic tactile  finding,  its  principal  factors  being  the  indifferent  con- 
ducting properties  of  the  lung,  diminished  resiliency  of  the  thorax, 
and  occlusion  of  the  bronchi  by  secretion  and  by  mucosal  swelling. 
In  some  instances  these  causes,  singly  or  combined,  are  capable  of 
entirely  cutting  off  the  transmission  of  voice  vibrations  to  the  chest- 
wall.  When  decided  bronchial  catarrh  coexists,  there  is  rhonchal 
fremitus.  Ordinarily  the  apex-beat  is  impalpable  at  its  normal 
site,  but  the  systolic  impulse  of  the  right  ventricle  can  be  felt  in  the 
epigastric  region.  Both  the  liver  and  the  spleen  may  be  so  large 
and  depressed  as  to  be  readily  palpable  below  the  costal  margin, 
and  over  the  former,  in  the  event  of  extreme  dilatation  of  the  right 
heart,  venous  pulsation  is  occasionally  appreciable.  Localized 
tenderness  and  pain  in  the  region  of  the  xiphoid  is  common,  this  so- 
called  "epigastric  spot"  of  pain  being  attributable  to  undue  pressure 
within  the  right  ventricle. 

Percussion. — The  percussion  sound  is  loudly  hyperresonant  and 
the  resistance  generally  is  increased  over  the  greater  part  of  both 
lungs,  but  especially  over  the  upper  lobes  anteriorly  are  these  char- 
acteristics most  clearly  demonstrable.  Strictly  speaking,  the  sound  is 
not  a  pure  tympany,  but  rather  tympany  ingrafted  upon  a  box-like 
tone — Biermer's  "band-box  resonance,"  or  a  commingling  of  vesicular 
resonance  and  tympany — Flint's  "vesiculo tympany."  Percussion  of 
the  pulmonary  borders  at  the  apices,  bases,  and  precordia  shows  that 
the  unnatural  resonance  extends  far  beyond  the  normal  limits  of  the 
lungs,  and  comparative  percussion  at  the  base  reveals  little  or  no 
inspiratory-expiratory  difference  in  the  levels  of  the  pulmonary 
borders,  indicating  restricted  excursion  of  the  emphysematous 
lungs.  The  encroachment  of  the  hyperresonance  diminishes  or 
entirely  obliterates  cardiac  dulness,  lowers  the  upper  levels  of  the 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         245 

hepatic  and  splenic  areas,  and  extinguishes  the  pure  gastric  tym- 
pany  of  Traube's  space. 

Auscultation. — Enfeeblement  of  respiratory  murmur,  with  low- 
pitched  and  notably  prolonged  expiration  and  short,  silent  inspira- 
tion, is  the  distinctive  auscultatory  finding.  Expiration,  whose 
duration  equals  or  exceeds  that  of  inspiration,  may  be  either  almost 
inaudible,  or,  if  bronchitis  and  asthma  coexist,  wheezy,  harsh,  and 
more  or  less  masked  by  bronchial  rales.  Over  the  distended  areas 
where  the  pulmonary  elasticity  persists  the  breath-sounds  are  vicari- 
ously exaggerated  and  puerile  in  character.  Vocal  resonance 
behaves  like  vocal  fremitus  (v.  s.).  A  peculiar  parchment-like 
crepitation,  audible  chiefly  at  the  apices  during  forced  inspiration, 
has  been  described  in  emphysema,  the  production  of  the  sound  being 
variously  referred  to  the  friction  between  subpleural  bullae  and  the 
costal  pleura  and  to  the  crackling  expansion  of  the  emphysematous 
tissue,  of  which  factors  the  former  appears  the  more  plausible.  As 
the  result  of  right  heart  failure,  the  liquid  bubbling  of  pulmonary 
edema  may  be  detected  at  the  bases  posteriorly.  The  cardiac  sounds, 
owing  to  the  interposed  lung,  are  distant  and  muffled,  and  with  the 
supervention  of  leakage  at  the  right  auriculoventricular  orifice,  a 
systolic  murmur  in  the  tricuspid  area  develops.  The  pulmonic 
second  sound  is  accentuated  during  the  phase  of  right  ventricular 
hypertrophy,  but  weakens  progressively  as  this  chamber  becomes 
inadequate  and  finally  dilates. 

Diagnosis. — Habitual  cough,  dyspnea,  and  cyanosis  with  bilateral 
thoracic  distention,  hyperresonance,  a  vertical  type  of  respiration, 
and  unduly  prolonged  low-pitched  expiration  admit  of  but  one 
interpretation. 

Simple  chronic  bronchitis,  while  it  may  give  rise  to  cough,  dyspnea, 
and  somewhat  prolonged  expiration,  is  not  attended  by  enlargement 
and  increased  resonance  of  the  thorax,  so  long  as  it  is  unaccom- 
panied by  emphysema. 

Pneumothorax,  like  emphysema,  is  attended  by  cough,  labored 
breathing,  and  signs  of  defective  blood  aeration,  but  in  the  former 
the  attack  is  most  sudden  and  its  severity  most  alarming,  while  in  the 
latter  the  symptoms  develop  gradually  and  are  not  so  urgent.  The 
physical  signs  of  pneumothorax  differ  from  those  of  emphysema  in 
being  unilateral,  not  bilateral;  the  increased  resonance  more  often 
amounts  to  pure  tympany  than  to  ordinary  hyperresonance;  the 
respiratory  and  voice-sounds,  if  not  wholly  abolished,  are  amphoric 
and  echoing,  instead  of  being  merely  enfeebled  or  wheezy.  More- 
over, air  within  the  pleural  cavity  causes  most  conspicuous  visceral 
displacement,  and,  when  associated  with  a  liquid  effusion,  is  betrayed 


246  PHYSICAL    DIAGNOSIS 

by  several  distinctive  signs — Hippocratic  succussion  sound,  metal- 
lic tinkling,  and  basal  flatness.  Should  air  escape  into  the  pleural 
cavity  from  an  emphysematous  lung,  the  physical  signs  of  the  latter 
condition  will  be  suddenly  replaced,  on  the  side  of  the  pleural  per- 
foration, by  those  of  acute  pneumothorax. 

ATROPHIC   EMPHYSEMA   (Small  lunged  Emphysema  j    Senile  Atrophy  of   the 

Lungs) 

This  affection  is  essentially  a  senile  atrophy  of  the  lungs,  which 
eventually  shrink  to  a  surprisingly  small  volume,  and  are  converted 
into  a  mass  of  atrophic,  functionless  tissue  permeated  by  air-spaces 
of  various  size,  constructed  of  dilated,  wasted,  and  ruptured  infundib- 
ula  and  air-vesicles.  The  atrophied  lungs  are  commonly  the  seat 
of  deep  pigmentation,  and  are  not  infrequently  affected  by  local 
fibrosis,  congestion,  edema,  and  infarction.  Progressive  atrophy 
of  the  thoracic  muscles  accompanies  the  pulmonary  wasting,  until 
finally  the  chest,  in  strong  contrast  to  that  of  hypertrophic  emphy- 
sema, becomes  abnormally  small,  and  the  course  of  the  ribs  extremely 
oblique,  thus  diminishing  the  thoracic  diameters  and  capacity,  and 
creating  an  acute  subcostal  angle;  the  respiratory  movements  are 
about  equally  restricted  during  both  phases  of  respiration.  The 
heart,  like  the  lungs,  is  atrophied — it  is  not  subject  to  undue  stress, 
and,  therefore,  neither  hypertrophies  nor  dilates. 

The  physical  signs  differ  somewhat  in  detail  from  those  of  large- 
lunged  emphysema.  The  dyspnea  is  inspiratory-expiratory,  not 
chiefly  expiratory;  vocal  fremitus  is  more  likely  to  be  exaggerated 
than  enfeebled;  the  hyperresonance  is  often  modified  by  fibroid 
deposits  at  the  apices  and  by  congestive  and  edematous  changes  at 
the  bases.  Owing  to  the  pulmonary  shrinkage  the  limits  of  the  lungs 
are  contracted,  and  in  consequence  there  is  an  apparent  increase  in 
the  extent  of  the  cardiac  and  hepatic  dulness,  though  both  the 
heart  and  the  liver  actually  may  be  smaller  than  normal. 

The  diagnosis  of  atrophic  emphysema  usually  can  be  made  at 
a  glance,  by  noting  the  size  and  shape  of  the  thorax  and  the  evidences 
of  senile  changes  elsewhere.  Chronic  cough  and  moderate  dyspnea 
attend  the  development  of  the  atrophic  alterations. 

COMPENSATORY  EMPHYSEMA   (Collateral.  Complementary.  Viearioof. 
or  Local  Emphysema) 

When  a  circumscribed  part  of  the  lung  is  rendered  impervious  to 
air,  other  areas  suffer  undue  inspiratory  distention,  in  an  endeavor 
to  compensate  for  the  loss  of  aerating  surface  in  the  crippled  part, 
and  the  overinflated  pulmonary  tissue  upon  which  this  extra  work 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         247 

is  imposed  is  said  to  be  in  a  state  of  compensatory,  complementary, 
or  vicarious  emphysema.  The  distended  vesicles  contain  a  consider- 
able excess  of  air,  and  it  frequently  happens  that  this  excess  is  not 
entirely  expelled  by  the  expiratory  efforts,  owing  to  some  bron- 
chiolar  obstruction,  by  secretion  or  by  a  turgid  mucosa,  sufficient 
to  prevent  the  free  exit  of  air,  but  not  necessarily  interfering  with  its 
entrance.  Thus,  the  intravesicular  tension  becomes  progressively 
increased,  and  the  air-cells  more  and  more  stretched,  until,  finally, 
should  the  underlying  cause  persist,  permanent  dilatation,  with 
structural  changes  like  those  of  true  hypertrophic  emphysema,  is 
established.  If,  on  the  contrary,  the  factor  of  this  vicarious  distention 
is  removed  before  the  pulmonary  elasticity  is  impaired  and  the 
vesicles  irreparably  damaged,  their  temporary  overinflation  entails 
no  subsequent  derangement  of  function. 

Circumscribed  vesicular  dilatation  takes  place  in  the  sound  lung 
adjacent  to  areas  of  atelectasis,  fibrosis,  tuberculosis,  and  other 
lesions  provocative  of  local  airlessness  of  the  pulmonary  tissues,  and 
in  wide-spread  adhesive  pleurisy  a  corresponding  degree  of  vicarious 
dilitation  exists,  especially  along  the  anterior  borders  of  the  lungs. 
Compensatory  emphysema  of  an  entire  lung  is  usually  traceable  to 
extensive  cirrhosis,  large  pleural  effusion,  massive  pneumonia,  or 
pneumothorax  of  the  opposite  lung.  As  already  intimated,  the 
extent,  character,  and  permanence  of  a  compensatory  dilatation  of 
the  lungs  stands  in  direct  relation  to  the  nature  and  the  duration  of 
the  underlying  cause. 

The  physical  signs  over  the  affected  area  or  areas  vary  with  the 
extent  of  the  process  and  the  structural  alterations  wrought  thereby. 
If  there  be  simple  acute  dilatation  with  increased  elasticity  of  the 
lung,  as  is  often  the  case,  hyperresonance,  a  harsh  puerile  respiratory 
murmur,  with  little  or  no  prolongation  of  its  expiratory  phase,  and 
exaggeration  of  vocal  fremitus  and  resonance  are  the  findings.  If 
the  process  be  of  longer  standing,  impairing  the  contractile  power  of 
the  lung,  the  signs  are  similar  to  those  of  generalized  hypertrophic 
emphysema,  restricted  to  the  part  implicated.  The  diagnosis 
depends  not  so  much  upon  these  signs,  which,  unfortunately,  are 
in  many  instances  obscure,  as  it  does  upon  the  patient's  history  and 
the  detection  of  some  satisfactory  cause  of  the  compensatory  process. 

ACUTE  VESICULAR  EMPHYSEMA  (Acute  Pulmonary  Distention) 

In  certain  cases  of  urgent  dyspnea  a  sudden  bilateral  hyperdis- 
tention  of  the  lungs  sometimes  occurs,  due  in  part  to  excessive  inspir- 
atory  stretching  of  the  vesicles  and  in  part  to  expiratory  stress.  The 
condition  is  one  of  simple  functional  pulmonary  distention  unat- 


248  PHYSICAL    DIAGNOSIS 

tended  by  atrophic  changes  in  the  vesicular  walls,  the  increased 
volume  of  the  lungs  depending  entirely  upon  a  generalized  dilatation 
of  the  air-cells.  This  so-called  acute  vesicular  emphysema  may 
develop,  with  striking  abruptness,  during  acute  diffuse  bronchitis, 
bronchial  asthma,  pertussis,  or  cardiorenal  disease,  and  in  tracheal 
and  laryngeal  stenoses.  The  sprinter's  "  second  wind, "  says  White- 
locke,  is  presumably  an  acute  type  of  physiologic  emphysema,  due 
to  violent  exercise.  The  physical  signs  are  similar  to  those  of  hyper- 
trophic  emphysema,  save  that  the  right  heart  shows  no  evidences 
of  habitual  strain.  (Cf.  Acute  Pulmonary  Tympanites,  p.  145.) 

INTERSTITIAL  EMPHYSEMA   (InUrlobular  or  Intervesicular  Emphysema) 

Interstitial  emphysema,  or  an  accumulation  of  air  in  the  stroma 
of  the  lung,  arises  when,  in  consequence  either  of  trauma  or  of  violent 
expiratory  strain,  air  escapes  through  a  breach  in  the  intervesicular 
walls  into  the  intervesicular  and  interlobular  tissues,  where  it  collects 
in  the  form  of  bubbles  ranging  in  size  from  about  a  millimeter  to  a 
centimeter  or  larger.  These  bubbles  of  air,  if  not  absorbed,  may 
work  through  the  interstitial  tissues  to  the  surface  of  the  lung,  where 
they  persist  as  little  globules  or  as  larger  bullae,  freely  movable 
beneath  the  pleura;  exceptionally,  the  air  burrows  from  the  root  of 
the  lung  into  the  mediastinum  and  thence  upward  along  the  trachea 
into  the  subcutaneous  structures  of  the  neck  and  the  thoracic  wall; 
or — and  this  also  is  uncommon — the  pleura  may  be  perforated  and 
spontaneous  pneumothorax  produced.  Air  entering  through  a 
tracheotomy  wound  sometimes  travels  downward  through  the  peri- 
tracheal  and  peribronchial  tissues,  ultimately  collecting  in  the  sub- 
pleural  connective  tissue.  Apart  from  that  variety  due  to  wounds 
of  the  lung,  interstitial  emphysema  is  referable  to  alveolar  rupture 
caused  by  violent  fits  of  coughing,  and  by  the  excessive  intrapulmonary 
tension  incident  to  convulsions,  parturition,  and  straining  at  stool. 

Physical  signs  of  interstitial  emphysema  are  usually  lacking,  and 
the  condition  is  discovered  more  often  at  autopsy  than  clinically. 
When  the  cellular  tissue  of  the  neck  is  infiltrated  with  air,  one  some- 
times detects  a  subcutaneous  emphysematous  swelling  which,  on 
palpation,  affords  a  curious  sort  of  crackling  sensation,  while  it  has 
been  asserted  that  a  peculiar  "crumpling  friction-sound"  can  be 
heard  over  a  collection  of  subpleural  beads  of  air. 

ATELECTASIS    (Pulmonary  Collapse;  Apneumatosis) 

Clinical  Pathology. — Atelectasis,  or  collapse  of  the  lung,  is  met 
with  either  as  an  acquired  condition  or  as  a  congenital  defect,  the 
latter  being  of  but  little  interest  to  the  internist.  Acquired  atelectasis 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         249 

» 

is  due  to  factors  depriving  the  lung  of  its  normal  content  of  air  and 
effectually  preventing  its  reinflation,  either  by  obstructing  the  passage 
of  air  through  the  bronchi,  by  actual  compression  of  the  pulmonary 
structure,  or  by  persistent  inadequacy  of  expansion.  Obstruction 
atelectasis  is  secondary  to  bronchial  obstruction  with  absorption 
of  the  air  in  the  vesicular  territory  beyond,  and  this  type  of  pulmo- 
nary collapse  is  referable  to  occlusion  of  the  bronchial  lumen  by 
mucosal  swelling,  viscid  secretion,  membrane,  blood-clot,  calculus, 
aspirated  foreign  bodies,  cicatrices,  and  new-growths;  or  bronchial 
stricture  due  to  external  pressure,  glandular,  neoplastic,  or  aneuris- 
mal,  may  be  the  underlying  cause  of  the  atelectatic  lesion.  Com- 
pression atelectasis  arises  when  the  lung  is  subjected  to  pressure, 
such  as  that  exerted  by  large  pleural  and  pericardial  effusions  of 
liquid,  pneumothorax,  hypertrophy  of  the  heart,  and  aneurism  or 
morbid  growth  of  the  thorax;  less  commonly  the  pressure  is  sub- 
phrenic,  as  in  the  case  of  a  large  abdominal  tumor  or  effusion,  whereby 
the  diaphragm  is  displaced  upward  and  crowded  against  the  pul- 
monary bases;  and  in  the  exceptional  instance  the  compression  is 
traceable  to  a  crooked  spine  or  to  a  deformed  chest-wall.  A  variable 
degree  of  atelectasis,  from  habitual  vesicular  underinflation,  also 
attends  inadequate  expansion  of  the  lungs,  whether  due  to  simple 
shallow  breathing,  to  prolonged  dorsal  decubitus,  or  to  diminished 
irritability  of  the  respiratory  center. 

Congenital  atelectasis,  met  with  in  prematurely  born  and  in  weakly 
full-term  infants,  is  characterized  by  imperfect  inflation  of  the  lungs 
after  birth,  owing  to  feeble  respiratory  movements  or  to  bronchial 
occlusion  by  aspirated  secretion.  This  type  of  vesicular  collapse  is 
either  disseminated  in  numerous  areas  throughout  both  lungs,  or 
implicates  the  greater  part  of  a  lobe  or  even  of  an  entire  lung,  in  the 
last  event  meriting  the  title  apneumatosis. 

The  appearance  of  an  atelectatic  lung  varies  with  the  extent  and 
the  chronicity  of  the  process  (Fig.  109).  Multiple  small  foci  of 
collapse,  such  as  those  incident  to  catarrhal  pneumonia,  show  beneath 
the  pleura  as  depressed  blue  or  purple  spots,  each  surrounded  by 
a  paler  zone  of  vicariously  dilated  vesicles.  An  extensive  area  of 
diffuse  collapse,  due,  for  example,  to  the  pressure  of  a  large  pleural 
effusion,  consists  of  tough,  dense,  airless  tissue,  gray  or  of  a  light  pink 
hue,  and  perhaps  limited  and  bound  down  by  fibrous  bands  and  by 
a  thickened,  contracted  pleura.  The  lung  above  the  seat  of  atelectasis 
is  compensatorily  distended,  and  should  the  collapse  be  wide-spread, 
the  lung  is  pushed  upward  and  backward  against  the  spinal  column. 
If  the  cause  be  speedily  removed  and  no  inflammatory  complications 
develop,  the  atelectatic  area  or  areas  may  reinflate  and  the  normal 


250 


PHYSICAL    DIAGNOSIS 


function  of  the  vesicles  be  completely  restored,  but  if  the  collapse 
persists,  irreparable  damage  to  the  lung  occurs,  and  the  deflated  part 
becomes  permanently  deprived  of  air.  In  the  latter  event  the  com- 
pressed and  intimately  opposed  intervesicular  septa  undergo  infiltra- 
tion with  blood,  whereby  the  affected  part  is  converted  into  a  dark, 


Bronchi 


Atelectatic  and  carnified  area 
Fig.  109. — Pulmonary  atelectasis  (Jefferson  Hospital  Laboratories). 

pulpy  patch  of  splenization;  later  the  epithelium  of  the  air-cells  degene- 
rates, and  the  vesicles  become  coalescent  and  matted  together  by 
newly  proliferated  cellular  tissue  until,  finally,  the  atelectatic  focus 
is  transformed  into  a  mass  of  the  consistence  and  general  appearance 
of  raw  beef — pulmonary  carnification.  Subsequently  this  carnified 
tissue  organizes,  forming  in  the  course  of  time  a  firm,  contracted, 
pigmented  patch  of  cirrhosis.  As  a  rule,  there  are  thickening  and 
adhesion  of  the  pleurae  adjacent  to  an  atelectatic  lesion,  and  the 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        251 

bronchial  tubes  passing  through  it  are  inflamed,  dilated,  and  other- 
wise altered  structurally. 

Physical  Signs. — The  physical  signs  of  atelectasis  are  intimately 
blended  with  those  of  the  exciting  cause  of  the  change,  as,  for  example, 
the  coexisting  catarrhal  pneumonia,  pleural  effusion,  or  enlarged 
heart,  and,  furthermore,  they  are  determined  by  the  extent  and  the 
situation  of  the  atelectatic  area,  as  well  as  by  the  secondary  change? 
existing  therein  and  in  the  adjacent  lung. 

Inspection. — In  extensive  atelectasis  there  is  extreme  respiratory 
distress,  as  shown  by  the  subject's  rapid,  shallow  breathing,  cyanosis, 
and  inspiratory  recession  of  the  lower  thorax  and  epigastrium. 
Indeed,  in  many  instances  these  dyspneic  phenomena  are  practically 
all  that  one  finds,  for  deeply  seated  areas  of  collapse,  if  not  far  beyond 
the  range  of  percussion  and  auscultation,  produce  signs  whose  identity 
is  masked  by  the  attendant  compensatory  emphysema  and  bronchial 
sounds. 

Palpation. — Collapsed,  toneless  pulmonary  tissue,  being  a  poor 
conductor  of  vibrations,  weakens  vocal  fremitus,  but  when  the  deflated 
area  undergoes  consolidation  and  becomes  denser,  the  fremitus  is 
clearly  transmitted  if  not  exaggerated.  Pleural  friction  sometimes 
may  be  felt  when  the  condition  of  the  pleurae  is  such  that  they  grate 
noisily  with  the  respiratory  excursions. 

Percussion. — As  a  rule,  there  is  nothing  more  than  emphysematous 
hyperresonance,  save  in  the  case  of  a  circumscribed  compact  lesion 
near  the  surface  of  the  lung;  this,  of  course,  impairs  pulmonary 
resonance,  and  sometimes  affords  typical  dulness,  with  undue  plexi- 
meter-finger  resistance.  If  tightly  compressed  against  a  large  patent 
bronchial  tube,  a  large  patch  of  atelectatic  lung  may  give  a  tympanitic 
note,  since,  to  all  intents  and  purposes,  the  bronchus  is  an  air-con- 
taining cavity,  whose  tone  traverses,  unaltered,  the  adjacent  dense 
and  airless  pulmonary  tissue. 

Auscultation. — The  respiratory  murmur  is  generally  suppressed, 
or  quite  lost,  but  over  a  dense  peribronchial  patch  bronchovesicular 
or  typical  bronchial  breathing  may  be  heard.  Provided  that  some 
air  enters  the  collapsed  vesicles,  a  few  crepitant  and  subcrepitant 
rales  are  audible  toward  the  end  of  deep  inspiration.  In  bed-ridden 
subjects,  with  no  pulmonary  disease,  atelectatic  crepitations  over  the 
bases  and  the  anterior  borders  of  the  lungs  are  very  common,  as  the 
result  of  prolonged  recumbency  which,  by  interfering  with  adequate 
vesicular  inflation,  has  allowed  collapse  and  mural  agglutination 
of  some  of  the  air-cells.  With  deep  inspiration,  however,  the  col- 
lapsed vesicles  inflate,  with  the  production  of  audible  crepitations 
as  their  sticky  walls  separate.  (See  p.  164.) 


252  PHYSICAL   DIAGNOSIS 

Diagnosis. — As  a  foregoing  paragraph  suggests,  in  many  instances 
the  diagnosis  of  atelectasis  must  needs  be  inferential  rather  than 
evidential,  being  based  upon  such  findings  as  respiratory  distress, 
hyperresonance,  and  signs  of  some  condition  causative  either  of  bron- 
chial obstruction  or  of  pulmonary  compression.  Small  foci  of  col- 
lapse, even  if  numerous,  give  no  tangible  symptoms  whatever  so 
long  as  they  are  well  compensated  by  the  coexisting  vesicular  dilata- 
tion. A  dense  circumscribed  area  of  atelectasis  furnishes  the  signs  of 
consolidation — exaggerated  fremitis,  bronchophony,  harsh  or  tubu- 
lar respiration,  and  dulness,  if  the  communicating  bronchi  remain 
open;  respiratory  silence  and  dulness,  if  the  bronchi  be  plugged. 

Here  may  be  noted  the  lesion  of  acute  lobar  atelectasis,  due  to 
diphtheritic  paralysis  and  to  reflex  inhibition  of  the  phrenic  move- 
ments after  surgical  operations;  less  commonly  acute  lobar  collapse 
results  from  pneumothorax  and  from  obstruction  of  the  air-pas- 
sages. In  this  "active  lobar  collapse  of  the  lung,"  described 
by  William  Pasteur,  the  main  features  include  the  abrupt  on- 
set of  dyspnea,  cyanosis,  and  thoracic  pain  attended  by  moder- 
ate cough  and  considerable  greenish  sputum;  the  physical  signs 
point  to  unilateral  lobar  collapse,  associated  with  a  notable 
dislocation  of  the  heart  toward  the  affected  side.  As  a  rule,  these 
active  symptoms  persist  for  but  a  brief  period,  and  the  deflated 
lung  regains  its  former  functionating  power  within  a  few  days. 

Atelectatic  solidification  is  differentiated  from  croupous  pneu- 
monia by  the  absence  of  a  distinctive  pneumonic  symptom-com- 
plex, and  by  contrasting  the  history  and  course  of  the  two  affec- 
tions and  the  associated  pulmonary  changes  incident  thereto. 

PNEUMONOCONIOSIS 

Clinical  Pathology. — A  combined  fibrosis  and  pigmentation  of 
the  lungs,  due  to  the  inhalation  of  minute  particles  of  dust,  is  known 
as  pneumonoconiosis,  of  which  general  process  there  are  numerous 
special  types,  corresponding  to  the  character  of  the  aspirated  material. 
Thus,  anthracosis  (coal-miner's  lung;  black  phthisis)  is  common 
among  miners  and  stokers,  who  habitually  breathe  an  atmosphere 
heavily  charged  with  pulverous  carbon  (Fig.  no).  Siderosis  (knife- 
grinder'e  phthisis;  grinder's  asthma)  results  from  the  inhalation  of 
fine  particles  of  metal,  especially  iron  and  steel;  this  form  of  pneu- 
monoconiosis particularly  affects  grinders  and  polishers,  who 
are  exposed  to  the  clouds  of  metal  dust  produced  by  the  abrasion 
of  metallic  surfaces  by  a  grindstone.  Chalicosis  or  lithosis  (grinder's 
rot;  stone-cutter's  phthisis)  is  due  to  the  inhalation  of  mineral  dusts 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        253 


inseparable  from  the  trades  of  stone-cutting,  dressing,  and  polishing ; 
to  some  extent  those  who  suffer  from  siderosis  also  acquire  more  or 
less  chalicosis,  from  breathing  the  fine  dust  abraded  from  the  sur- 
face of  the  grindstone.  Kaolinosis  (potter's  lung)  develops  from  the 
aspiration  of  the  dust  of  kaolin,  a  plastic  clay  used  in  making  pottery. 
Millers,  as  well  as  those  who  handle  tobacco,  cotton,  flax,  furs,  and 
other  organic  materials,  are  subject  to  inhalation  cirrhoses  from  dust 
irritation.  Of  the  preceding  varieties  of  pneumonoconiosis,  that 
due  to  soot  or  coal-dust  is  the  least  destructive,  and  though  a  miner's 
lung  may  be  densely  carbonized  throughout,  severe  structural  changes 
do  not  necessarily  develop  in  consequence.  Furthermore,  it  is  unques- 
tionably a  fact  that  anthracosis  confers  a  relative  immunity  to  pul- 
monary tuberculosis.  The  sharp,  gritty  particles  of  pulverized  metal 
and  stone  are  much  more  harmful,  and  lead  not  only  to  extensive 
interstitial  fibrosis,  but  also  predispose  to  tuberculous  infection  of 
the  lungs,  especially  in  the  case  of  metal  infiltrations.  Oliver  has 
drawn  attention  to  the  disas- 
trous inroads  of  Rand  miners' 
phthisis  among  gold  miners 
in  the  Transvaal  who  breathe 
air  charged  with  quartz  dust, 
and  Robertshaw  has  empha- 
sized the  high  mortality  of 
ganister  miners'  disease,  or  a 
form  of  phthisis  secondary 
to  pneumoconiosis  affecting 
miners  of  ganister,  a  flinty 
mineral  composed  chiefly  of 
silica.  The  dusts  of  wool,  fur, 
hair,  and  other  organic  sub- 
stances are  practically  always 
contaminated  by  bacteria, 
and,  therefore,  are  most  likely 
to  cause  serious  destructive 
processes,  as  well  as  inter- 
stitial fibrosis.  Apart  from 
their  mechanical  irritation, 
certain  dusts  also  have  a 

Chemic    action,     and    to     this   Fig.  no. -Pulmonary    anthracosis    (Jefferson 
...  .  Hospital  Laboratories). 

peril    those    engaged   in    the 

manufacture  of  paints,  hats,  and  wall-paper  are  exposed,  by  being 
forced  to  breathe  air  full  of  dust  charged  with  mercury,  lead,  or 
arsenic,  as  the  case  may  be. 


254  PHYSICAL    DIAGNOSIS 

No  one's  lungs  are  wholly  free  from  dust,  it  is  true,  but  ordinarily 
little  or  none  of  it  reaches  the  pulmonary  interstices,  for  the  coarser 
particles  are  excluded  by  the  cilia  of  the  upper  air-passages,  while 
finer  dust  deposited  in  the  trachea  and  bronchi  is  there  incorporated 
with  secretion  or  ingulfed  by  mucous  and  alveolar  cells  and  subse- 
quently expelled  by  the  action  of  the  ciliated  epithelium  and  by 
coughing  and  expectoration.  But  these  protective  measures,  though 
adequate  under  ordinary  circumstances,  fail  to  prevent  excessive 
deposits  of  finely  granular  inspirated  material  within  the  lungs  of  per- 
sons who  day  after  day  are  compelled  to  inhale  heavily  dust-laden 
air.  Under  such  conditions  numerous  dust-particles  escape  removal 
from  the  air-tubes,  and,  either  naked  or  phagocyted,  penetrate  the 
mucosa,  whence  they  enter  the  lymph-spaces  and  are  carried 
by  the  lymphatics  permanently  to  lodge  in  the  intervesicular 
and  bronchiolar  tissues  and  in  the  thoracic  lymphatic  glands. 
Especially  abundant  are  the  particles  deposited  in  the  peribronchial 
and  periarterial  lymphatic  nodules,  in  the  tissues  of  the  interlobular 
septa  under  the  pleura,  and  in  the  substernal,  tracheal,  and  bron- 
chial glands.  Ordinarily,  the  granules  go  no  farther  than  these 
adenoid  structures,  but  exceptionally  peribronchial  glandular  adhe- 
sions to  the  pulmonary  veins  open  the  door  to  the  general  circulation, 
with  consequent  pigmentation  of  the  liver  and  spleen. 

In  all  probability  visceral  pigmentation  is  also  due,  at  least  to  some 
extent,  to  the  transference  of  ingested  dust-particles  from  the  alimen- 
tary tract  to  the  blood-stream,  via  the  lymphatics  and  the  thoracic 
duct,  and,  furthermore,  the  same  mechanism  accounts  for  some  of 
the  pulmonary  deposits,  though  to  a  distinctly  minor  degree. 

Although  the  pulmonary  stroma  can  harbor  an  extraordinarily 
large  amount  of  grit  and  other  foreign  particles  for  a  long  period 
without  being  damaged  thereby,  in  time  they  irritate,  provoke  pro- 
liferation of  the  connective-tissue  elements,  and  hence  cause  fibrous 
overgrowth.  This  process  in  the  glands  leads  finally  to  their  complete 
sclerosis,  while  the  fibrous  thickening  of  the  intervesicular  walls 
results  in  destruction  of  their  blood-vessels  and  in  obliteration  of 
the  air-vesicles,  the  affected  tissues  being  thus  deprived  of  air.  As 
a  rule,  the  cirrhosis  begins  in  the  peribronchial  tissues,  but  ultimately 
it  tends  to  invade  other  areas  the  fusion  of  which  converts  the  lung 
into  a  more  or  less  generally  indurated  mass;  the  infiltrations  are 
likely  to  be  most  extensive  and  dense  near  the  pulmonary  apices. 
The  lesions  appear  as  scattered  or  diffuse  patches  of  indurated,  air- 
less tissue  traversed  by  thickened,  catarrhal  bronchial  passages,  and 
surrounded  by  a  zone  of  emphysematous  lung.  Their  color  varies 
with  the  character  of  the  infiltrated  material — jet  black,  grayish 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        255 

black,  or  slate  color  in  the  anthracotic  lung;  brick  red  or  black  in 
siderosis ;  and  steel  gray  or  unduly  pale,  perhaps  with  brown  stains 
or  stipples  of  altered  blood-pigment,  in  chalicosis.  Sometimes  the 
fibroid  territories  become  necrotic  and  cavernous  (Charcot's  ulceres 
du  poumon) ,  and  sometimes  the  cavities  erode  into  a  nearby  bronchus, 
whereupon  infection  takes  place,  with  rapid  enlargement  of,  and  sup- 
puration within,  the  excavation.  Implication  of  the  bronchial  tree, 
in  the  form  of  chronic  bronchitis  with  mural  thickening,  invariably 
attends  the  foregoing  changes;  emphysema  generally  develops  in  the 
course  of  time;  in  some  instances  there  are  bronchiectases;  and  a 
variable  amount  of  pleural  thickening  and  adhesion  commonly 
ensues.  The  right  side  of  the  heart  is  enlarged  as  the  result  of  the 
cirrhotic  process,  and  not  uncommonly  the  organ  is  dislocated  by 
fibrous  traction. 

Physical  Signs. — The  physical  signs  of  pneumonoconiosis  are  those 
of  chronic  bronchitis,  emphysema,  and  chronic  fibroid  induration 
of  the  lungs,  associated  in  some  instances  with  bronchiectasis  and 
with  chronic  ulcerative  phthisis.  The  sputum,  which  may  contain 
tubercle  bacilli,  usually  is  abundant,  and  of  mucopurulent,  some- 
times fetid,  character.  It  is  blackened  by  coal-dust  particles  in 
anthracosis,  reddened  by  bits  of  oxid  of  iron  in  siderosis,  and 
shows  fine  silicate  granules  under  the  microscope  in  chalicosis. 

Diagnosis. — In  a  person  whose  occupation  necessitates  the  in- 
halation of  dust,  a  history  of  years  of  bronchitis  and  emphy- 
sema ultimately  followed  by  progressive  cirrhosis  of  the  lung,  together 
with  the  distinctive  appearance  of  the  sputum,  is  unmistakable 
evidence  of  pneumonoconiosis.  Signs  of  pulmonary  phthisis  are 
also  obvious  in  some  cases,  particularly  in  siderosis. 

PULMONARY   ABSCESS    (Purulent  Pneumonia) 

Clinical  Pathology. — Pulmonary  abscess  may  arise  in  the  various 
forms  of  aspiration  pneumonia  from  infected  particles  sucked  into 
the  finer  bronchi,  wherein  the  contaminating  material  lodges  and 
excites  a  suppuration  which  extends  to  the  contiguous  vesicular  struc- 
tures. Occasionally,  croupous  pneumonia  terminates  in  suppuration 
of  the  lung,  and,  less  commonly,  this  serious  accident  follows  ordinary 
catarrhal  pneumonia.  Abscess  of  the  lung  due  to  the  extension 
of  some  primary  focus  of  infection,  either  by  contiguity  or  by  the 
lymphatics,  is  a  potential  complication  in  phthisis,  pneumonoconiosis, 
bronchiectasis,  empyema,  mediastinal  abscess,  esophageal  cancer, 
hepatic  abscess,  and  suppurating  hydatid  cyst  of  the  lung  or  the 
liver.  Stab  wounds  of  the  chest-wall,  or  even  a  presumably  sterile 


256  PHYSICAL   DIAGNOSIS 

paracentesis,  may  carry  pyogenic  infection  to  the  pulmonary 
tissue.  In  pyemic  conditions  the  origin  of  pus  foci  in  the  lungs 
is  traceable  to  emboli  laden  with  pus-germs  lodged  in  the  termi- 
nal branches  of  the  pulmonary  artery. 

Pulmonary  suppuration  may  take  the  form  of  a  solitary  abscess 
of  variable  size,  of  multiple  abscesses  usually  of  small  size,  or  of 
diffuse  purulent  infiltration.  If  of  moderate  extent,  the  purulent 
area  sometimes  is  walled  off  from  the  surrounding  lung  by  an  imperme- 
able fibrous  capsule,  but,  on  the  other  hand,  practically  an  entire 
lobe  may  be  invaded  by  a  huge  solitary  abscess,  developing  either 
by  the  progressive  spread  of  the  primary  focus  or  by  the  coalescence 
of  several  small  points  of  pus.  An  abscess  of  the  lung  begins  as  an 
intense  suppurative  pneumonitis  followed  by .  softening,  necrosis, 
and  sloughing  of  the  infected  pulmonary  tissue  which,  in  consequence, 
undergoes  excavation.  The  wall  of  the  cavity,  inclosing  a  collection 
of  pus  and  disintegrated  pulmonary  tissue,  is  lined  at  first  with  ragged 
remnants  of  the  necrotic  lung  and  with  inflammatory  tissue,  but 
later  this  lining  ordinarily  is  replaced  by  a  smooth  pyogenic  mem- 
brane, the  contiguous  lung  being  consolidated  by  infiltration  and  by 
a  variable  degree  of  fibrosis.  Outside  this  none  too  firm  a  barrier 
the  lung  is  more  or  less  engorged,  edematous,  and  hemorrhagic. 
Apart  from  the  possibility  of  being  isolated  by  encapsulation,  a  small 
abscess  may  ultimately  heal  by  absorption  of  the  purulent  matter 
and  by  cicatrization,  but,  on  the  contrary,  the  infection  may  spread 
to  other  parts  of  the  lung.  Drainage  is  sometimes  established  by 
erosion  into  a  bronchus;  or  the  pus  may  invade  the  pleural  cavity 
and  cause  empyema.  Infected  emboli  giving  rise  to  small,  usu- 
ally numerous,  wedges  of  pus  lying  base  toward  and  close  to  the 
pleura,  are  an  especially  common  factor  of  this  accident.  It  should 
be  added  that  empyema  is  also  attributable  to  infection  through 
pleural  membranes  permeable  by  bacteria,  but  intact  in  the  sense 
that  no  actual  breach  exists  therein.  Exceptionally,  a  channel  is 
worn,  via  an  abscess  cavity,  between  a  bronchial  tube  and  the  pleura, 
and  under  this  circumstance  pyopneumothorax  almost  inevitably 
supervenes.  Pus  diffused  through  the  interstices  of  the  lung,  without 
the  formation  of  circumscribed  abscess,  is  accounted  for  by  dissemi- 
nation of  pyogenic  microorganisms  by  the  lymph-stream. 

Physical  Signs. — Abscess  of  the  lung  affords  definite  thoracic 
signs  only  when  it  is  of  comparatively  large  size  and  superficial  situa- 
tion, in  which  event  the  objective  signs  of  pulmonary  consolidation 
and  excavation  are  appreciable,  together  with  corroborative  evidence 
such  as  dyspnea,  cough,  "pump-handle"  pyrexia,  sweats,  and  emaci- 
ation. Signs  of  bronchitis  and  of  pleurisy,  both  frequent  concomitant 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        257 

lesions,  are  commonly  demonstrable,  and  in  certain  cases  it  is  not 
difficult  to  find  some  primary  affection,  either  within  or  remote 
from  the  lungs,  to  explain  the  pulmonary  suppuration.  The  sputum 
is  generally  profuse,  has  a  nauseatingly  sweet  and  heavy  odor,  is  of 
purulent  character,  and  may  contain,  in  addition  to  pus-cells  and 
bacteria,  shreds  of  elastic  fiber  and  necrotic  tissue  from  the  lung. 
Copious  gushes  of  expectoration  sometimes  occur  when  the  secretion 
rising  within  an  abscess  cavity  overflows  into  the  bronchial  outlet 
and  in  so  doing  provokes  a  fit  of  so-called  "evacuative  cough." 
When  the  suppurative  process  is  composed  of  multiple  small  foci  or 
is  diffusely  infiltrated,  no  clear  physical  signs  can  be  looked  for,  and 
under  these  circumstances  the  symptoms  of  septic  intoxication  rule 
the  clinical  picture. » 

Diagnosis. — The  character  of  the  sputum,  a  clinical  picture  of 
septic  poisoning,  and  physical  signs  of  pulmonary  softening  and 
excavation  appearing  as  a  sequel  to  a  primary  lesion  of  the  lung  are 
the  cardinal  points  of  diagnosis.  Empyema  may  be  attended  by 
constitutional  symptoms  like  those  of  pulmonary  abscess,  and,  should 
the  purulent  matter  be  discharged  through  a  bronchus,  the  patient 
may  suddenly  cough  up  mouthfuls  of  pus,  either  practically  pure  or, 
rarely,  fetid,  but  quite  free  from  elements  derived  from  disintegration 
of  the  lung.  This  fact,  with  the  discovery  of  fluid  in  the  pleura,  shows 
the  pleural  origin  of  the  pus.  Abscess  versus  gangrene  of  the  lung 
is  referred  to  under  the  latter  affection.  (See  p.  260.) 

PULMONARY   GANGRENE    (Necropneumonia;   Pulmonary  Sphacela- 
tion  or  Mortification) 

Clinical  Pathology. — A  dual  factor  is  at  work  in  producing 
gangrene  of  the  lung:  diminished  vitality  of  the  pulmonary  tissue  and 
infection  of  the  devitalized  part,  the  former  being  due  to  inadequate 
blood-supply  and  the  latter  to  the  invasion  of  pyogenic  and  associated 
bacteria.  Subnormal  tissue  resistance  must  be  regarded  as  the 
essential  predisposing  cause  of  gangrene,  and  this  serves  to  explain 
the  relative  frequency  of  this  grave  affection  in  persons  whose  nutri- 
tion and  defensive  powers  have  been  lowered  by  diabetes,  alcoholism, 
chronic  debility,  and  exhausting  fevers,  and  its  rarity  in  those  whose 
health  has  not  been  undermined.  Bacterial  infection  of  vascularized 
pulmonary  tissue  generally  means  nothing  more  than  abscess,  at 
least  primarily,  but  when  the  tissue's  blood-supply  is  cut  off,  infec- 
tion induces  mortification.  Important  causes  of  pulmonary  gangrene 
include  aspiration  and  croupous  pneumonias,  abscess,  cancer,  and 
tuberculosis  of  the  lung,  bronchiectasis,  and  bronchial  stenosis  by 
17 


PHYSICAL   DIAGNOSIS 


foreign  body  or  by  pressure  of  an  aneurism  or  neoplasm,  and  con- 
tamination by  some  extrapulmonary  necrotic  process.  Pulmonary 
embolism,  particularly  when  septic,  is  likely  to  set  up  tissue  death  in 
the  infarcted  area  beyond  the  clot,  and  this  factor  explains  the  occa- 
sional development  of  pulmonary  gangrene  in  abscess  of  the  middle 
ear,  the  mastoid,  or  the  brain,  in  ulcerative  endocarditis,  in  femoral 
thrombosis,  and  in  acute  febrile  infections.  Less  commonly,  sterile 
emboli  account  for  a  gangrenous  lung. 

Pathologically,  there  are  two  well-defined  types  of  pulmonary 
gangrene:  the  circumscribed  and  the  diffuse.  Circumscribed  gan- 
grene may  consist  either  of  a  single  area  or  of  multiple  foci  of  dead 
pulmonary  tissue  of  reddish-brown,  greenish,  or  black  appearance, 
and  sharply  delimited  from  the  neighboring  inflamed  lung  (Fig.  in). 

As  the  tissue  disintegra- 
tion and  solution  proceed, 
the  gangrenous  patch 
softens  and  is  converted 
into  an  excavation  with 
rough,  shaggy  walls  in- 
closing a  fetid  semifluid 
mass  of  necrotic  debris. 
Bronchi  near  or  within 
such  a  cavity  are  fre- 
quently eroded,  and  in 
consequence  furnish  an 
outlet  for  the  putrescent 
material,  and  arteries 
traversing  a  gangrenous 
area  become  thrombotic 
and  perhaps  so  worn  that 
free  hemorrhage  takes 
place.  The  pulmonary 
tissue  around  a  circum- 
scribed gangrenous  lesion 
is  extremely  hyperemic, 
and  more  or  less  solidified  by  infiltration  and  by  edema.  As  in  abscess 
of  the  lung,  a  subpleural  spot  of  gangrene  excites  pleural  inflamma- 
tion, thickening,  and  adhesion,  and  if  the  membranes  be  perforated, 
empyema,  sometimes  pyopneumothorax,  supervenes.  Intense  bron- 
chitis, generally  of  the  putrid  type,  and  inflammatory  swelling 
of  the  bronchial  glands  are  common  complications  of  pulmonary 
gangrene.  Aspirated  particles  of  fetid  bronchial  secretion  may  excite 
gangrenous  bronchopneumonia  in  either  the  affected  or  the  opposite 


Fig.  in. — Gangrene  of  the  lung   (Jefferson  Hos- 
pital Laboratories). 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        259 

lung.  In  some  instances  the  mediastinum,  the  pericardium,  or  the 
abdomen  is  contaminated  by  the  process  of  erosion,  and  embolic 
transference  of  the  infection  is  not  unlikely  to  occur,  producing  lesions 
of  distant  organs,  for  example,  abscess  of  the  brain.  Diffuse  gangrene 
of  the  lung,  lacking  the  sharp  line  of  demarcation  so  distinctive  of 
the  circumscribed  form,  sometimes  arises  by  extension  of  the  latter, 
or  it  may  be  a  primary  diffuse  process  consequent  to  pneumonia, 
bronchiectasis,  putrid  bronchitis,  or  pulmonary  artery  thrombosis. 
The  greater  part,  if  not  the  whole,  of  a  lobe  is  transformed  into  a 
black  or  greenish  mass  of  putrid  necrosis,  farthest  advanced  in  the 
center  of  the  lesion,  whence  the  destructive  changes  gradually  blend 
with  those  of  the  surrounding  inflamed  and  consolidated  lung.  The 
diseased  tissue  at  first  is  of  firm,  solid  consistence,  but  later  it  becomes 
soft,  pultaceous,  and  riddled  with  communicating  cavities  of  various 
size.  Fatal  septicemia,  septic  thrombosis,  hemorrhage,  or  pyopneu- 
mothorax  is  the  sequel  to  be  expected  in  this  type  of  pulmonary 
gangrene. 

Physical  Signs. — Little  can  be  learned  from  examination  of  the 
lungs  unless  the  gangrenous  area  be  extensive  and  near  the  surface, 
when,  like  abscess,  it  produces  the  physical  signs  of  pulmonary 
solidification,  softening,  and  excavation.  Furthermore,  it  is  almost 
invariably  the  rule  also  to  find  evidences  of  intense  bronchial  inflam- 
mation, pleurisy,  and  other  attendant  lesions  either  provocative  of, 
or  consequent  to,  the  rotting  lung.  When  a  gangrenous  area  com- 
municates with  a  bronchus,  the  patient's  breath  becomes  horribly 
fetid  and  the  sputum  abundant,  thin,  and  usually  of  a  dirty  greenish- 
brown  hue.  The  sputum,  too,  smells  vilely,  for  it  reeks  with  decom- 
posed tissue,  pus,  and  putrefactive  bacteria.  On  standing,  it  tends 
to  separate  into  three  layers:  a  dark  granular  sediment,  a  middle 
zone  of  thin  liquid,  and  a  top  layer  of  mucopus.  Microscopically, 
aside  from  shreds  of  necrotic  pulmonary  tissue  and  perhaps  elastic 
fibers,  the  sputum  ordinarily  shows  pus  and  red  blood-cells,  blood- 
pigment,  Dittrich's  plugs,  fat-globules  and  fatty  acid  crystals,  choles- 
terin,  leucin  and  tyrosin,  swarms  of  bacteria,  and,  exceptionally, 
flagellate  organisms  and  sarcinae. 

Diagnosis. — The  fetor  of  the  breath  and  the  character  of  the 
sputum  are  the  two  most  distinctive  features  of  pulmonary  gangrene, 
which  in  typical  instances  is  also  attended  by  physical  signs  of  pul- 
monary disintegration,  by  moderate  fever  and  rapid  pulse,  by  dyspnea, 
cough,  and  sometimes  hemoptysis,  by  emaciation  and  prostration, 
and,  in  certain  cases,  by  delirium.  When  the  subject  gives  a  history 
of  diabetes  or  other  debilitating  disease  and  has  suffered  from  some 
acute  pulmonary  lesion  prior  to  the  onset  of  this  pertinent  symptom 


260  PHYSICAL   DIAGNOSIS 

group,  the  diagnosis  is  reasonably  certain.  On  the  other  hand,  not 
infrequently  the  diagnosis  of  gangrenous  lung  must  be  made  more  by 
inference  than  by  clinical  proof,  for  in  some  instances  there  is  neither 
foul  breath  nor  necrotic  sputum;  in  others  these  two  diagnostic 
mainstays  are  referable  to  some  non-gangrenous  lesions;  and  in  still 
others  there  are  indefinite  chest  signs,  or  none  at  all.  Thus,  in  the 
condition  termed  latent  pulmonary  gangrene,  met  with  particularly 
in  diabetics  and  in  the  insane,  the  patient's  breath  is  untainted  and 
the  sputum  odorless  and  mucoid,  probably  because  the  lung  necrosis, 
though  sometimes  extensive,  progresses  leisurely,  is  well  circumscribed, 
and  does  not  open  into  a  bronchus.  In  a  case  of  this  sort,  affording 
possibly  nothing  but  a  suspicious  history  and  signs  of  consolidation, 
an  antemortem  diagnosis  of  gangrene  is  not  possible.  Stinking 
breath  and  fetid  expectoration  may  arise  from  purulent,  decomposing 
lesions  of  the  bronchi,  lungs,  and  pleural  cavity,  without  the  coexist- 
ence of  gangrene. 

In  pulmonary  abscess  the  breath  is  foul,  but  the  odor  is  distinctively 
sweetish  and  not  so  fetid  and  heavy  and  penetrating  as  in  gangrene; 
while  the  sputum,  frequently  coughed  up  in  copious  gushes,  consists 
chiefly  of  pus,  though  it  occasionally  contains  shreds  of  disintegrated 
lung. 

In  putrid  bronchitis  the  breath  is  horribly  fetid — only  theoretically 
less  so  than  in  gangrene — but  the  foul  sputum,  abundant  and  sero- 
purulent,  does  not  contain  pulmonary  shreds  nor  elastic  fibers. 

Bronchiectasis  taints  the  subject's  breath  with  an  odor  of  putre- 
faction only  a  shade  less  offensive  and  permeating  than  gangrene. 
This  is  true,  notably,  of  saccular  bronchiectases  characterized  by 
the  periodic  discharge  of  large  quantities  of  sputum  charged  with 
putrescent  matter  and  pus,  but  generally  free  from  elastic  fibers, 
save  in  the  event  of  bronchial  ulceration. 

Advanced  pulmonary  tuberculosis,  with  cavities  full  of  decomposing 
secretion,  may  be  responsible  for  fetid  breath  and  for  foul  sputum 
containing  elastic  fibers,  but  the  breath,  despite  its  disagreeable 
odor,  has  not  the  vile  smell  of  gangrene,  the  sputum  is  filled  with 
tubercle  bacilli,  and  the  patient  usually  shows  unmistakable  signs 
of  apical  excavation  and  of  systemic  inroads  by  the  infection. 

Bad  breath  incident  to  ozena  and  to  alveolar  necrosis  obviously 
can  be  identified  by  examination  of  the  nose  and  the  mouth. 

PULMONARY  NEOPLASMS 

Carcinoma. — Carcinoma,  the  most  frequent  type  of  pulmonary 
neoplasm,  is  rarely  of  primary  origin,  for  the  lung  is  usually  invaded 
by  the  transference  of  a  neoplastic  process  from  an  adjacent  or  a 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        261 

distant  initial  lesion.  In  Stevens's  analysis  of  more  than  32,000 
autopsies  by  various  foreign  reporters  only  43  cases  of  primary 
pulmonary  cancer  are  recorded.  The  tumor,  commonly  an 
encephaloid,  may  be  situated  in  a  neighboring  structure,  such 
as  the  pleura,  esophagus,  breast,  or  mediastinum,  or  in  some 
remote  part,  like  the  liver,  gastro-intestinal  canal,  or  uterus, 
whence  bits  of  the  original  tumor  are  carried,  by  the  lymph 
or  blood,  to  the  lung,  therein  to  lodge,  proliferate,  and  replace 
the  pulmonary  tissue.  A  lung  may  also  be  attacked  by  a  can- 
cer originating  in  the  mucous  glands  of  the  bronchi  or  possibly 
in  the  alveolar  epithelium  and  eventually  spreading  through 


Fig.  112. — Radiograph  of  a  pulmonary  neoplasm.     Anterior  aspect,  showing  shadow 
of  growth  in  left  lung.     (Plate  by  Dr.  W.  F.  Manges.) 

both  lungs.  Bilateral  implication  is  the  rule  in  growths  of  secondary 
type,  and  in  primary  cancer  the  tumor  may  either  be  confined  to 
the  lung  originally  affected,  or  spread  to  the  other  lung  and  to  nearby 
structures.  Primary  carcinoma  of  the  lung  is  decidedly  more  fre- 
quent in  men  than  in  women,  and  the  lesion  in  many  instances 
appears  to  be  directly  attributable  to  trauma;  cobalt  miners  are 


262  PHYSICAL   DIAGNOSIS 

supposed  to  be  exceedingly  predisposed.  Of  the  two  sexes,  women 
are  the  more  susceptible  to  secondary  cancer. 

Malignant  growths  of  the  lung  primarily  cripple  the  organ's  res- 
piratory function  by  replacing  the  normal  pulmonary  tissue,  and 
subsequently,  as  the  neoplastic  consolidation  progresses,  necrotic 
changes  are  prone  to  supervene  both  in  the  malignant  areas  and  in 
other  parts  of  the  lung.  In  an  extreme  instance  virtually  an  entire 
lung  is  invaded  by  the  new-growth,  ordinarily  by  the  coalescence 
of  numerous  foci  multiplying  by  local  metastases  from  the  parent 
lesion,  but  exceptionally  arising  by  a  more  diffuse  extension,  radially 
or  eccentrically,  from  the  original  deposit.  In  the  immediate  vicinity 
of  the  neoplastic  areas  the  lung  is  collapsed,  carnified,  and  edematous, 
and  in  other  parts  the  vesicles  are  compensatorily  dilated.  When  a 
malignant  mass  impinges  closely  against  a  bronchus,  atelectasis  and 
its  unfortunate  consequences  arise  in  the  corresponding  vesicular 
territory;  when  a  bronchus  is  perforated,  bits  of  tumor  tissue  may 
enter  the  tube,  to  be  coughed  up  and  expectorated,  or  to  be  aspirated 
into  other  bronchial  twigs,  therein  exciting  bronchopneumonic  proc- 
esses and  also  secondary  foci  of  the  original  tumor.  Malignant 
areas  communicating  with  a  bronchial  tube  are  most  susceptible  to 
bacterial  infection,  and  hence  to  gangrenous  degeneration  and  excava- 
tion, while  the  same  thing  may  happen  to  patches  of  consolidated 
inflamed  lung  similarly  situated.  The  growth  may  compress  the 
gullet,  the  superior  vena  cava,  the  internal  mammary  artery,  or  the 
pulmonary  vessels,  giving  rise  to  pressure  symptoms  similar  to  those 
found  in  mediastinal  tumor.  Pleural  inflammation,  setting  up  adhe- 
sions and  thickening  or  attended  by  effusion,  often  of  hemorrhagic 
character,  is  inevitable  when  the  malignancy  reaches  the  surface  of 
the  lung.  In  the  rare  event  of  pleural  perforation  pneumothorax, 
of  course,  ensues.  With  the  extension  of  the  malignant  process 
beyond  the  confines  of  the  lung,  invasion  of  the  tracheobronchial, 
mediastinal  and  cervical  glands,  the.  pleural  membranes,  and  the 
opposite  lung  is  the  natural  sequence. 

The  physical  signs  of  pulmonary  carcinoma  naturally  are  subject 
to  wide  variance  in  the  individual  case,  according  to  the  site  and 
size  of  the  neoplastic  infiltration  and  the  bronchopulmonary  damage 
thereby  caused.  Cachexia,  though  more  or  less  apparent,  tends 
to  develop  more  slowly  and  less  conspicuously  in  cancer  of  the  lung 
than  in  cancer  elsewhere  situated.  The  superficial  veins  of  the  neck 
and  thoracic  wall  may  be  distended  abnormally  in  consequence 
of  pressure  upon  the  superior  cava  and  internal  mammary  vein. 
The  respiratory  mobility  of  the  affected  side  is  sometimes  restricted 
and  the  contour  of  the  chest  altered,  being  bulged  and  intercostally 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        263 

widened  by  a  massive  growth,  and  retracted  by  one  attended  by  dense 
fibrosis  and  adhesions  or  by  pressure  atelectasis.  Vocal  fremitus 
is  very  variable,  being  determined  chiefly  by  the  conducting  properties 
of  the  neoplasm  and  the  state  of  the  surrounding  vesicular  structure. 
Dulness  is  afforded  by  a  large,  diffuse,  superficial  tumor;  hyperreso- 
nance  or  tympany,  by  a  cancerous  excavation  within  range  of  the 
percussion  strokes;  and  wooden  flatness,  by  extensive  pleural  implica- 
tion. Abnormalities  of  the  respiratory  murmur  include  suppressed 
breathing,  due  to  a  moderately  disseminated  growth;  loud  tubular 
respiration,  produced  by  a  large  compact  infiltration;  and  the  amphoric 
tone  of  a  cavity.  Various  rales,  of  bronchial,  vesicular,  and  pleural 


Fig.  113. — Sarcoma  of  the  lung  (Jefferson  Hospital  Laboratories). 


origin,  are  audible  when  there  is  coexistent  bronchitis,  congestion, 
edema,  or  pleurisy. 

Sarcoma. — As  a  pulmonary  growth  sarcoma  is  distinctly  less  com- 
mon than  carcinoma,  and,  save  in  exceptional  instances,  is  of  second- 
ary development,  the  initial  tumor,  according  to  West,  existing  in 
bone  in  one-third  of  all  cases.  Hypernephroma  is  followed  by 
pulmonary  metastasis  of  sarcomatous  type  in  fully  60  per  cent. 


264  PHYSICAL   DIAGNOSIS 

of  cases  (Wooley).  As  a  rule,  the  growth  is  disseminated  through 
both  lungs.  Pulmonary  sarcoma  is  peculiar  in  two  details:  the 
long  interval  that  may  elapse  in  secondary  cases  between  the  ap- 
pearance of  the  initial  tumor  and  its  metastasis  in  the  lung,  and 
its  frequency  in  advanced  life  rather  than  in  youth.  A  primary 
sarcoma  of  the  lung,  which  usually  is  unilateral,  is  a  very  rare  lesion, 
and  commonly  consists  of  an  endothelioma  originating  in  the  pleura, 
or,  exceptionally,  in  the  lymph-follicles  or  blood-vessels. 

The  physical  signs  of  pulmonary  sarcoma  do  not  differ  from  those 
of  the  other  type  of  malignant  disease  of  the  lung  discussed  above, 
and,  therefore,  need  not  be  further  discussed. 

ACTINOMYCOSIS 

Pulmonary  actinomycosis,  though  rare,  is  of  clinical  interest 
because  of  its  more  or  less  close  resemblance  to  certain  other 
pulmonary  diseases,  notably  tuberculosis.  The  ray-fungus  may 
invade  the  lung  primarily,  or  may  extend  thereto  by  metastasis, 
by  bronchogenic  infection  from  a  buccal  lesion,  or  by  direct 
extension  from  a  neighboring  focus.  The  process  is  essentially 
chronic,  progressively  destructive,  and  most  unlikely  to  become 
arrested.  Ordinarily,  it  is  characterized  by  chronic  diffuse  bronchitis, 
attended  by  fetid  mucopurulent  sputum  charged  with  actinomycelic 
granules.  In  such  instances  bronchopneumonic  lesions  some- 
times develop,  from  the  inhalation  of  contaminated  matter,  and  set 
up  a  so-called  miliary  type  of  the  disease,  resembling  in  its  general 
features  miliary  tuberculosis.  The  growth  of  fungous  nodules 
in  the  lungs  leads  ultimately  to  obliteration  of  the  vesicular  structures 
and  induces  a  condition  of  exudative  catarrhal  pneumonia;  suppura- 
tion, softening,  and  excavation  of  the  actinomycotic  area  occur; 
and  in  some  cases  perinodular  fibrosis  develops,  which  not  only  has 
a  tendency  to  encapsulate  the  specific  lesions,  but  also  to  spread 
through  the  adjacent  interalveolar  tissues.  Thus,  the  greater  part 
of  an  actinomycotic  lobe  may  be  converted  into  a  dense  fibrous  mass, 
riddled  with  pus-cavities,  traversed  by  fistulous  tracts,  and  stippled 
with  less  mature  foci  in  different  phases  of  development.  Extension 
of  the  process  toward  the  pleura  produces  inflammation  and  adhesion 
thereof,  and,  in  the  course  of  time,  after  the  invasion  of  these  mem- 
branes, the  chest-wall  may  become  implicated  or  the  abdominal 
cavity  penetrated. 

The  physical  signs  of  pulmonary  actinomycosis  are  in  no  sense 
distinctive,  for  usually  they  resemble  those  of  a  stubborn  catarrhal 
bronchitis,  of  a  chronic  bronchopneumonia  with  softening  and  excava- 
tion, or  of  an  abscess  of  the  lung.  Phthisis  in  its  various  phases  is 


DISEASES    OF    THE   BRONCHOPULMONARY    SYSTEM        265 

most  often  counterfeited,  sometimes  with  surprising  fidelity,  by  the 
general  clinical  picture,  but  in  such  a  contingency  the  true  nature 
of  the  symptoms  is  surely  revealed  by  examination  of  the  sputum. 
This  contains  the  characteristic  actinomyces  granules  ("  sulphur 
granules"),  consisting  of  minute  yellow-brown  or  gray  grains,  which, 
when  crushed,  are  found  to  be  made  up  of  an  obscure  central  gran- 
ular mass,  from  which  radiate  straight  and  undulating  threads  of 
mycelia,  many  showing  club-like  swellings. 

ECHINOCOCCUS  CYST 

The  lung  or  the  pleura,  particularly  the  former,  is  affected  in 
about  8  per  cent,  of  all  cases  of  echinococciasis,  the  lesion  com- 
monly being  secondary  to  an  hepatic  hydatid  which  has  ruptured 
through  the  diaphragm  or,  exceptionally,  reached  the  lung  by  way 
of  the  hepatic  vein,  inferior  cava,  and  right  heart.  The  development 
of  a  single  cyst  in  one  lung  is  more  frequent  than  the  growth  of  mul- 
tiple cysts,  either  unilaterally  or  bilaterally,  and  in  most  cases  the 
lower  right  lobe  is  the  seat  of  the  lesion.  As  the  size  of  the  cyst  or 
cysts  increases,  corresponding  compression  of  the  lung  is  provoked, 
and  the  tumor  may  dislocate  the  mediastinal  structures,  encroach 
upon  the  pleural  sac,  and  depress  the  diaphragm.  Death  of  the 
cyst  is  likely  to  induce  inflammatory  changes  resulting  in  suppura- 
tion, gangrene,  and  cavity  formation;  or  the  cyst  fluid  may  become 
absorbed  and  inspissated,  the  wall  atrophy,  and  the  process  undergo 
encapsulation  by  lime  salts.  So  long  as  a  hydatid  lives  and  grows 
and  remains  of  moderate  size,  neither  irritation  nor  inflammation 
of  the  lung  is  likely  to  supervene.  Should  a  cyst  rupture,  it  generally 
does  so  into  a  bronchus,  whereupon  purulent  material,  bits  of  cyst 
membrane,  booklets,  and  free  blood  may  be  expectorated;  less 
commonly  it  bursts  into  the  pleura,  causing  pyopneumothorax;  and 
exceptionally  it  suppurates  through  the  chest-wall. 

Physical  signs  are  not  demonstrable  until  the  cyst  attains  consider- 
able size,  excites  inflammatory  changes,  or  ruptures.  Suggestive, 
but  not  distinctive,  signs  include  cough,  dyspnea,  hemoptysis,  local 
bulging,  restricted  breathing,  and  a  circumscribed  dull  area  over 
which  vocal  fremitus,  vocal  resonance,  and  respiratory  sounds  are 
impaired  or  abolished.  The  heart  and  the  liver  may  be  displaced, 
and  not  uncommonly  there  are  evidences  of  bronchitis,  pulmonary 
consolidation,  and  pleural  effusion.  Over  a  large  superficial  cyst 
it  is  sometimes  possible  to  detect  hydatid  fremitus  and  sonorous 
hydatid  resonance  (q.  v.).  Eosinophilia  is  an  important  sign  of 
early,  active  echinococciasis.  Exploratory  puncture  may  give  the 
correct  clue  to  a  puzzling  group  of  physical  signs,  and  the  sputum 


266  PHYSICAL   DIAGNOSIS 

sometimes  affords  pathognomonic  findings,  such  as  booklets  and 
laminated  membrane.     (See  p.  59.) 

PLEURISY   (Pleoritis) 

The  term  pleurisy  is  applicable  to  numerous  types  of  acute  and 
chronic  pleural  inflammation  that  differ  greatly  in  extent,  intensity, 
and  character,  according  to  the  circumstances  prevailing  in  the 
individual  instance.  The  lesion  may  be  confined  to  a  circumscribed 
area,  or  implicate  the  greater  part  of  the  pleural  surfaces;  its  pre- 
dominant character  is  fibrinous,  serofibrinous,  or  purulent;  and  its 
origin  is  more  frequently  secondary  and  symptomatic  than  pri- 
mary or  idiopathic.  For  clinical  study  it  is  convenient  to  recognize 
the  following  main  types  of  pleural  inflammation,  although,  patho- 
logically, such  clear-cut  distinctions  are  not  always  warranted: 
(a)  Acute  fibrinous  pleurisy,  (b)  Serofibrinous  pleurisy,  (c)  Puru- 
lent pleurisy,  (d)  Circutnscribed  pleurisy,  (e)  Chronic  adhesive 
pleurisy. 

By  far  the  greatest  number  of  cases  of  pleurisy  are  of  the  secondary 
or  symptomatic  type,  arising  most  commonly  from  the  extension  of 
inflammatory  diseases  of  the  lungs  and  adjacent  parts,  of  which 
lesions  tuberculosis  is  of  especial  importance.  Rarely  does  the 
pleura  escape  damage  in  this  disease,  though  not  always  does  it 
become  actually  tuberculous;  less  frequently  a  pulmonary  tuber- 
culosis is  lighted  up  by  a  primary  tuberculous  focus  of  the  pleura. 
To  the  group  of  pulmonary  factors  of  pleurisy  also  belong  pneumonia, 
infarction,  abscess,  gangrene,  and  neoplasm;  while  in  other  cases  the 
process  may  arise  by  extension  in  consequence  of  disease  of  the 
pericardium,  the  peritoneum,  the  liver,  or  the  bony  thorax.  Many 
pleurisies  are  traceable  to  such  underlying  conditions  as  rheumatic 
fever,  nephritis,  gout,  syphilis,  and  alcoholism. 

Of  primary  pleurisy,  a  comparatively  rare  condition,  there  is  little 
to  be  said.  A  small  minority  of  cases  correspond  to  this  caption — 
for  example,  those  developing  in  a  subject  of  low  vital  resistance 
after  exposure  to  cold  and  dampness;  but  many  apparently  primary 
pleurisies  are,  in  reality,  of  the  secondary  type,  though  the  under- 
lying factor  may  be  masked.  Bacteriologically,  the  tubercle  bacillus, 
the  pneumococcus,  and  the  streptococcus  are  the  three  bacteria 
principally  concerned  as  the  causes  of  various  forms  of  pleurisy, 
and  of  these  organisms  the  first  is  the  most  frequent  offender,  the 
second  the  least  harmful,  and  the  last  the  most  virulent.  Less  com- 
monly pleurisy  is  referable  to  other  microorganisms,  notably  to 
staphylococci,  pneumobacilli,  colon  bacilli,  typhoid  bacilli,  and  diph- 
theria bacilli. 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        267 

ACUTE    FIBRINOUS    PLEURISY    (Acute   Dry   or   Plastic    Pleurisy;    Pleuritis 

Sicca) 

Clinical  Pathology. — This  form  of  pleurisy,  which  is  more  often 
confined  to  one  or  several  circumscribed  areas  than  generally  dis- 
seminated, is  accompanied  by  little  or  no  accumulation  of  serum, 
the  inflamed  membranes,  after  a  primary  stage  of  acute  injection, 
being  coated  with  a  scanty  fibrinous  exudate  which  obscures  the 
normal  glistening  surface  of  the  pleura  and  renders  it  dull,  opaque, 
and  lusterless.  In  a  moderate  inflammation  with  trifling  prolifer- 
ation of  fibrous  tissue,  the  exudate  may  soon  undergo  fatty  degen- 
eration and  partial  absorption,  leaving  merely  small  pearly  patches 
of  pleural  thickening  to  mark  the  site  of  the  lesion.  If  the  inflam- 
mation be  more  active,  however,  the  inflamed  parts  are  covered  by 
an  abundant,  thick  lymph  deposit,  tending  rapidly  to  become  organ- 
ized and  thus  ultimately  to  agglutinate  the  opposed  pleural  surfaces 
into  a  permanent  fibrous  union. 

Physical  Signs. — Inspection. — In  order  to  ease  the  pain  the 
patient,  when  erect,  instinctively  lowers  the  shoulder  and  rekxes 
the  musculature  on  the  affected  side,  and  lies  thereupon  when 
confined  to  bed.  The  respiratory  movements  are  shallow  and 
the  diaphragm  shadow  is  obscured,  especially  on  the  pleuritic 
side;  the  breaths  come  and  go  in  an  uncertain,  jerky,  and  painful 
manner;  and  the  subject  suffers  from  persistent,  dry,  and  restrained 
cough.  These  objective  symptoms  of  pleuritic  pain  are  by  no  means 
constant,  for,  remarkable  as  it  may  seem,  the  patient,  despite  wide- 
spread pleural  inflammation,  may  complain  of  no  discomfort  what- 
ever. Dilatation  of  the  pupil  on  the  affected  side,  from  sympathetic 
nerve  irritation,  is  a  finding  of  some  suggestiveness. 

Palpation  and  percussion  are  usually  negative,  save  in  the  event  of 
an  abundant,  thick  exudate  which  may  enfeeble  vocal  fremitus, 
modify  the  percussion  resonance,  and  increase  the  tactile  resistance 
of  the  area  percussed.  Distinct  friction  fremitus  is  sometimes  pal- 
pable over  the  inflamed  pleural  surfaces. 

Auscultation. — Friction-sounds  are  audible  over  the  site  of  the 
lesion  during  the  first  few  days  of  the  disease,  after  which  they  dis- 
appear as  the  pleuritis  subsides,  usually  with  a  more  or  less  per- 
manent adhesion  of  the  inflamed  pleural  surfaces.  In  this  type  of 
acute  pleurisy  the  friction,  usually  most  distinct  during  inspiration, 
resembles  a  series  of  delicate,  crepitating,  jerky  sounds,  which,  apart 
from  their  dry,  superficial  character,  are  very  like  the  vesicular  crepita- 
tion. The  ordinary  auscultatory  site  of  pleural  friction  is  shown  by 
Fig.  90,  p.  167.  Pleuropericardial  friction  sounds,  generated  by 
the  cardiac  impact,  are  audible  when  the  pleural  surfaces  adjacent 


268  PHYSICAL   DIAGNOSIS 

to  the  pericardium  are  roughened.  (See  p.  168.)  The  vesicular 
murmur,  though  frequently  suppressed,  shows  no  definite  pathologic 
modification,  and  vocal  resonance  remains  of  normal  degree. 

Diagnosis. — The  characteristic  friction-sound  is  sufficient  for 
the  direct  diagnosis  of  acute  plastic  pleurisy,  irrespective  of  the 
patient's  cough,  respiratory  distress,  fever,  and  other  objective  symp- 
toms. Routine  chest  examinations  in  subjects  of  various  pulmonary 
disorders  will  reveal  a  surprisingly  large  number  of  unsuspected  pleuri- 
sies, whose  existence  has  provoked  neither  pain  nor  any  other  dis- 
comfort. It  was  doubtless  the  acute  type  of  dry  pleurisy  that  the 
great  Dutchman,  Boerhaave,  had  in  mind  when,  more  than  two 
centuries  ago,  he  spoke  of  "a  sharp  pricking  inflammatory  pain  in 
the  side,  greatly  increased  in  the  act  of  inspiration,  but  abated  in 
expiration,  or  by  holding  the  breath,"  and  when  he  referred  to  "a 
cough,  which  is  almost  incessant,  and  which,  exciting  great  pain, 
is,  therefore,  stifled  or  suppressed  by  the  patient." 

Having  discovered  a  pleural  inflammation,  it  is  important  to  decide, 
by  further  inquiry,  if  the  lesion  be  uncomplicated,  if  it  be  sympto- 
matic of  some  diathetic  state,  or  if  it  be  secondary  to  pulmonary 
pericardial,  hepatic,  or  peritoneal  lesion. 

Both  intercostal  neuralgia  and  pleurodynia,  in  so  far  as  pain  is 
concerned,  may  closely  simulate  dry  pleurisy,  but  in  neither  of  these 
conditions  is  there  friction  or  fever.  Intercostal  neuralgia  is  most 
commonly  found  in  women  who  suffer  from  other  nerve  pains  and 
are  of  the  neurotic  temperament,  and  the  pain,  which  is  lancinating 
and  aggravated  by  motion,  radiates  along  the  course  of  the  superficial 
branches  of  the  intercostal  nerves,  whose  points  of  exit  (in  the  para- 
sternal  and  axillary  lines  and  at  the  bend  of  the  ribs)  are  the  seat 
of  the  most  exquisite  pain  on  palpation. 

Pleurodynial  pain,  which  is  prone  to  occur  in  connection  with 
«jther  myalgic  symptoms,  is  also  intensified  by  motion,  but  it  can  be 
circumscribed  to  the  intercostal  muscles  by.  making  pressure  over 
the  interspaces.  In  the  exceptional  case  subphrenic  peritonitis  (q.  v.) 
is  the  source  of  friction-sounds  audible  over  the  lower  part  of  the 
thorax. 

SEROFIBRINOUS   PLEURISY   (Pleurisy  with  Effusion) 

Clinical  Pathology. — In  serofibrinous  pleurisy  the  primary 
changes  are  essentially  those  of  the  fibrinous  type  of  the  disease, 
except  that  they  are  usually  more  acute  and  more  widely  distributed; 
as  a  rule,  they  are  unilateral.  The  affected  surfaces  are  coated  with 
a  fibrinous  exudate  which,  in  some  instances,  consists  merely  of 
a  thin,  smooth,  pale  film,  and  in  others  of  a  thick,  buttery  deposit 


DISEASES    OF   THE   BRONCHOPULMONARY    SYSTEM        269 

of  shaggy,  ragged,  honey-combed  appearance.  Attending  these 
primary  changes  there  is  a  free  outpouring  of  inflammatory  exudate, 
which  gravitates  to  the  lowest  part  of  the  pleural  sac,  save  when, 
owing  to  the  existence  of  pleural  adhesions,  it  is  hemmed  in  at  a 
higher  level.  The  amount  of  exudate  poured  out  varies  within  the 
widest  limits  in  different  cases:  ordinarily 'it  ranges  approximately 
between  16  and  64  ounces  (480  and  1920  c.c.),  but  exceptionally  it  is 
decidedly  larger — 100  ounces  (3000  c.c.)  or  more,  or,  as  in  Lieber- 
meister's  unique  case,  245  ounces,  i.  e.,  7350  c.c.  The  exudate  is  com- 
posed of  a  coagulable  albuminous  fluid  containing  fibrin,  blood-cells, 
swollen  endothelial  cells,  uric  acid,  cholesterin,  and  sugar.  These,  as 
well  as  the  other  constituents  of  the  exudate,  have  been  described  in  a 
preceding  section.  (See  p.  53.)  If  the  fibrin  content  be  moderate, 
the  fluid  is  of  a  clear  straw  color  and  contains  white  fibrinous 
flocculi;  if  the  fibrin  be  excessive,  the  exudate  becomes  turbid  and 
is  filled  with  numerous  matted,  curd-like  masses  of  fibrin  which  tend 
to  adhere  to  the  pleural  surfaces  in  thick,  creamy  layers. 

The  term  hemorrhagic  pleurisy  is  used  when  the  exudate  con- 
tains sufficient  erythrocytes  obviously  to  tinge  it  pink,  red,  or  brown, 
such  a  change  not  becoming  appreciable  until  the  erythrocytes 
number  at  least  6000  to  the  cubic  millimeter  of  fluid  (Dieulafoy). 
Blood-stained  effusions  are  very  suggestive  of  tuberculosis  and  of 
cancer;  less  commonly  they  attend  cardiac,  renal,  and  hepatic  lesions, 
the  specific  febrile  infections,  the  several  hemorrhagic  diatheses,  and 
various  low  asthenic  states;  and  exceptionally  they  result  from  simple, 
though  most  intense,  pleuritis.  Hemorrhagic  pleurisy  is  sometimes 
referable  to  the  rupture  of  a  vessel  coursing  through  a  false  membrane 
organized  upon  the  site  of  a  recurrent  pleural  inflammation.  True 
hemorrhagic  pleurisy  must  be  distinguished  from  an  ordinary  sero- 
fibrinous  effusion  accidentally  tinged  with  blood  by  a  tear  in  the  lung 
made  by  an  aspirating  needle,  and  from  the  accumulation  of  pure 
blood  in  the  pleural  sac,  or  hemothorax  (q.  v.). 

So-called  chyliform  pleurisy,  distinguished  by  a  turbid  exudate 
of  milky  appearance,  is  met  with  in  exceptional  cases  of  both  sero- 
fibrinous  and  purulent  effusions,  as  the  result  of  extensive  fatty  changes 
in  the  cellular  elements  of  the  exudate.  which,  microscopically,  shows 
many  fat-globules,  fatty  leukocytes  and  endothelium,  and  cholesterin 
crystals.  Effusions  of  this  type  (hydrops  adipostis),  which  are  likely 
to  be  of  tuberculous  origin,  of  a  primarily  purulent  nature,  and  of 
chronic  duration,  are  to  be  distinguished  from  genuine  chylothorax 
(hydrops  chylosus),  or  the  presence  of  pure  chyle  within  the  pleural 
sac  (q.  V.). 

If  the  exudate  be  of  considerable  volume,  the  lower  part  of  the 


270  PHYSICAL    DIAGNOSIS 

overlying  lung  is  compressed,  collapsed,  and  perhaps  deprived  of  air 
and  blood,  while  the  pulmonary  tissue  above  this  zone  of  carnifica- 
tion  is  vicariously  overdistended ;  in  a  very  large  and  persistent  effusion 
the  pulmonary  carnification  may  attain  so  extreme  a  degree  that 
subsequent  restoration  of  the  lung  is  impossible.  The  mediastinum 
is  dislocated  toward  the  sound  side,  and  the  heart  undergoes  a  similar 
displacement.  The  apex,  though  shifted,  is  never  rotated  (Osier), 
and  its  normal  relative  position  to  the  base  is  not  altered.  The 
weight  of  a  large  effusion  causes  the  diaphragm  to  sag  abnormally 
low  and  restricts  its  respiratory  excursions;  if  right-sided,  the  effusion 
depresses  the  liver,  and  if  left-sided,  the  stomach,  the  transverse 
colon,  and  the  spleen.  In  some  instances  the  vascular  trunks  within 
the  thorax  are  considerably  pressed  upon  by  the  exudate.  After  the 
removal  of  the  exudate,  whether  by  absorption  or  by  aspiration,  there 
is  a  certain  amount  of  connective-tissue  formation  at  the  site  of  the 
lesion,  in  favorable  cases  amounting  to  little  more  than  a  grayish 
area  of  moderate  thickening  or  to  limited  adhesions  of  the  opposed 
pleural  surfaces. 

The  factors  of  serofibrinous  pleurisy  are  virtually  those  of  the 
fibrinous  form,  and,  therefore,  do  not  call  for  further  mention.  The 
importance  of  tuberculosis  as  an  exciting  cause,  however,  must  be 
especially  emphasized,  for  a  large  proportion  of  cases  are  tuber- 
culous, either  primarily  or  in  consequence  of  infection  from  foci 
in  the  lungs,  peritoneum,  or  other  parts  of  the  body. 

Physical  Signs. — Inspection. — The  sharp  pain  of  the  preexudative 
stage  excites  both  hurried  and  restricted  breathing,  which  later,  as 
the  inflamed,  sensitive  pleural  surfaces  are  bathed  in  the  exudate, 
gives  way  to  painless  dyspnea,  the  urgency  of  which  is  related  chiefly 
to  the  extent  of  the  effusion;  should  there  be  patches  of  dry  pleurisy 
elsewhere,  however,  painful  respiration  persists  despite  the  effusion. 

An  extensive  effusion  causes  moderate  distention  and  decided 
immobility  of  the  affected  side,  but  comparative  measurements  of 
the  two  halves  of  the  thorax  will  show  that  this  increase  of  volume 
is  actually  much  less  than  it  appears,  since  it  rarely  amounts  to  more 
than  i  or  i£  inches  (2.5  to  3.75  cm.).  The  lower  intercostal  spaces  are 
unduly  shallow  or  even  quite  effaced,  so  that  the  contour  of  the  lower 
chest  is  smooth  and  rounded.  In  some  patients  the  interspaces  are 
wider  than  normal,  but  in  young  children  they  may  be  distinctly 
narrowed,  by  reflex  contraction  of  the  intercostal  muscles — a  sign 
described  by  Przewelski.  The  respiratory  excursions  of  the  affected 
side  are  considerably  restricted  and  the  diaphragm  shadow  of  Litten 
is  correspondingly  abolished,  while  the  opposite  half  of  the  thorax 
shows  exaggerated  expansion,  as  a  matter  of  compensation.  Inspec- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        271 

tion  of  the  back  may  reveal  a  deviation  of  the  spine  toward  the  side 
of  the  effusion. 

The  cardiac  impulse  is  dislocated  upward  and  toward  the  unaffected 
side.  In  a  left-sided  effusion  it  may  be  visible  in  the  epigastrium 
or  to  the  right  of  the  sternum,  sometimes  as  far  outward  as  the  neigh- 
borhood of  the  right  midclavicular  line  and  as  high  as  the  fourth  or 
the  third  interspace;  should  the  apex  be  pushed  directly  behind  the 
sternum,  no  impulse  will,  of  course,  be  visible.  In  a  right-sided 


Fig.  114.— Radiograph  of  a  left  pleural  effusion.     (Plate  by  Dr.  W.  F.  Manges.) 

effusion  the  apex-beat  may  be  displaced  an  interspace  upward  and 
carried  outward  to  or  even  beyond  the  left  midclavicular  line.  C.  L. 
Greene  has  pointed  out  that  the  cardiac  impulse  approaches  the 
median  line  with  deep  inspiration,  and  recedes  therefrom  with  expira- 
tion, this  sign  being  especially  apparent  in  effusions  of  moderate  size. 
It  is  demonstrable  in  some  cases  on  ordinary  inspection,  but  is  more 
clearly  recognized  with  the  fluoroscope. 

Fluoroscopic  examination  shows  a  shadow  over  the  site  of  the 
effusion,   and  also  indefiniteness  of  the  costal  and  diaphragmatic 


272  PHYSICAL    DIAGNOSIS 

outlines,  with  abnormal  depression  and  limited  mobility  of  the 
latter.  The  lung  above  the  effusion,  if  unduly  dense,  casts  a 
correspondingly  dark  shadow,  and  the  heart  encroaches  upon  the 
unaffected  side.  The  shadows  cast  by  serofibrinous  and  by  purulent 
effusions  do  not  differ  in  density,  according  to  Williams. 

Palpation. — In  the  dry  stage  of  the  inflammation  the  voice-sounds 
are  unaltered,  but  occasionally  a  friction  .fremitus  is  appreciable 
on  palpation.  Enfeeblement  or  total  abolition  of  vocal  fremitus 
is  most  convincing  evidence  of  a  collection  of  fluid  within  the  pleura, 
but,  unfortunately,  this  sign  is  not  invariably  obtainable,  owing  to 
the  coexistence  of  factors  whereby  tactile  fremitus  is  exaggerated. 
Thus,  despite  the  presence  of  a  well-marked  effusion,  the  voice  vibra- 
tions may  be  transmitted  through  the  liquid  by  bands  of  adhesions 
or  by  a  bronchus  dislocated  against  the  chest-wall,  while  in  other 
instances  they  may  travel,  via  an  overresilient  parietes,  from  the  sound 
to  the  affected  side.  It  is  in  children  especially  that  persistence  of 
vocal  fremitus  is  not  to  be  regarded  as  incompatible  with  a  pleural 
effusion.  The  fremitus  is  exaggerated  over  the  site  of  the  compressed 
lung  above  the  effusion.  Normal  vocal  fremitus  reappears  as  the 
effusion  diminishes  in  volume,  except  over  areas  where  the  thickening 
of  the  pleura  is  sufficient  to  damp  the  vibrations  of  the  spoken  voice. 

Aside  from  showing  the  intensity  of  the  vocal  fremitus,  palpation 
is  useful  in  determining  differences  in  the  contour  and  the  expansion 
of  the  two  halves  of  the  chest,  in  locating  the  cardiac  impulse,  and 
in  ascertaining  the  level  of  the  lower  border  of  the  liver.  Reflex 
muscular  contraction  and  rigidity  below  the  twelfth  rib  on  the 
pleuritic  side  is  commonly  appreciable  (Ramond). 

Percussion. — As  an  exudate  accumulates  within  a  pleural  sac  the 
percussion  sound  below  the  upper  level  of  the  liquid  first  becomes 
impaired,  then  frankly  dull,  and  finally  flat,  as  the  fluid  replaces 
pulmonary  tissue.  These  auditory  percussion  signs  are  attended 
by  a  sense  of  increased  resistance  to  the  pleximeter  finger,  corre- 
sponding to  the  degree  of  airlessness  of  the  area  percussed,  and  in 
the  typical  case  becoming  so  extreme  that  the  finger  perceives  no 
trace  of  the  normal  parietal  resiliency;  under  such  circumstances 
the  flatness  acquires  a  high-pitched,  wooden  quality,  most  character- 
istic of  fluid.  Over  the  compressed  and  vicariously  distended  lung 
above  the  effusion  Skodaic  resonance  is  obtained. 

A  small  effusion  usually  affords  no  physical  signs  anteriorly,  being 
recognized  by  the  appearance  of  a  narrow  zone  of  basal  flatness 
posteriorly,  which  extends  from  the  spine  outward  toward  the  axilla, 
and  shows,  with  the  patient  in  an  upright  position,  an  upper  limit 
following  a  line  of  upward  convexity.  When  an  effusion  attains 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        273 

sufficient  volume  to  produce  signs  anteriorly,  its  earliest  effects  are  the 
substitution  of  flatness  for  normal  hepatic  dulness  on  the  right  side,  and 
for  normal  tympany  in  the  upper  part  of  Traube's  semilunar  space, 
according  to  the  side  affected.  Over  a  moderate  effusion,  reaching  as 
high,  say,  as  the  fourth  rib  anteriorly,  the  upper  level  of  the  flatness 
follows  an  undulating  line  curving  from  behind  forward,  somewhat 
in  the  outline  of  the  letter  S — Ellis's  "S-shaped  line  of  flatness" 
(Fig.  115).  Ellis's  line,  which  corresponds  to  the  line  of  contact 
between  the  exudate  and  the  overlying  lung,  is  lowest  at  the 
spine,  whence  it  runs  obliquely  upward  and  forward  in  an  S-shaped 
course  toward  its  summit  in  the  axilla,  thence  dropping  abruptly 
downward  and  forward  to  the  sternum,  where  it  terminates  at  a 
slightly  higher  level  than  that  of  its  spinal  extremity.  An  effusion 
large  enough  to  cause  the  foregoing  sign  usually  produces  either 
decided  vertical  extension  of  the  area  of  hepatic  flatness,  or  very 
definite  obliteration  of  Traube's  space,  and  more  or  less  lateral  and 
upward  dislocation  of  the  cardiac  area.  Persistence  of  tympany  in 
Traube's  area,  despite  signs  of  a  left-sided  effusion,  suggests  the 
formation  of  adhesions  whereby  the  fluid  is  prevented  from  gravi- 
tating to  the  bottom  of  the  pleural  sinus. 

Except  at  the  base,  where  defective  resonance  is  not  unlikely  to 
persist  indefinitely,  the  transition  from  flatness  to  impaired  reso- 
nance to  the  normal  pulmonary  percussion  sound  rapidly  progresses 
over  the  site  of  the  effusion  as  it  subsides.  Persistent  areas  of  flat- 
ness, with  absence  of  tactile  vibrations,  point  to  circumscribed  per- 
manent thickening  of  the  pleura.  Coinciden tally  with  the  above 
changes,  it  is  found  that  the  organs  displaced  by  the  effusion  recede 
to  their  physiologic  percussion  limits. 

Movable  flatness,  due  to  change  in  the  posture  of  the  patient,  is 
rarely  demonstrable  in  simple  pleural  effusion,  and  in  those  excep- 
tional instances  in  which  the  change  does  occur  the  differences 
in  the  height  of  the  flatness  are  very  slight  and  of  slow  appearance. 
On  the  contrary,  when  the  pleura  contains  both  fluid  and  air,  as  in 
hydropneumothorax,  shifting  flatness  is  readily  determined.  In 
attempting  to  gage  differences  in  the  upper  level  of  flatness  by  com- 
parison of  the  surface  markings  of  this  limit  in  the  erect  and  the 
recumbent  positions,  it  is  well  to  remember  that  the  normal  stretching 
of  the  skin  when  the  subject's  posture  is  altered  shifts  marks  made 
thereon,  and  that  apparent  postural  differences  in  levels  of  flatness 
are  often  referable  merely  to  this  resiliency  of  the  integument. 

Grocco's  sign,  or  the  presence  of  a  triangular  area  of  shifting  dulness 
at  the  posterior  thoracic  base  opposite  the  effusion,  is  a  practically 
constant  indication  of  free  fluid  within  the  pleural  sac  (Fig.  115). 

18 


274 


PHYSICAL   DIAGNOSIS 


This  paravertebral  dulness  attends  both  small  and  large  free  effusions, 
and  can  also  be  detected  in  encapsulated  pockets  of  fluid  lying  close 
to  the  spine;  it  cannot  be  demonstrated  in  interlobar  pleurisy. 
Grocco's  sign  has  been  attributed  partly  to  mutation  of  the  vertebral 
vibrations  by  the  pressure  of  the  fluid  against  the  spine,  and  partly 
to  dislocation  of  the  mediastinum  toward  the  unaffected  side.  As 
a  rule,  the  dull  area  is  larger  in  effusions  of  the  right  than  in  those 
of  the  left  pleural  cavity. 

In  order  to  outline  Grocco's  triangle,  the  upper  limit  of  the 
effusion  and  the  lower  limit  of  normal  pulmonary  resonance  on 
the  opposite  side  are  first  ascertained,  with  the  patient  in  the 


Dulness 
(Grocco's  triangle)! 


Upper  level  of  effusion 
(Ellis's  line) 


Flatness 


Fig.   115. — Grocco's  paravertebral  dulness  in  pleural  effusion.     Arrows  indicate  per- 
cussion lines  to  be  followed  in  mapping  out  the  dull  area. 

erect  posture.  The  triangle  itself  is  mapped  out  by  percussing 
downward  over  the  spine,  horizontally  inward  along  lines  paral- 
lel to  the  spine,  and  obliquely  inward  toward  the  spine,  sur- 
face markings,  to  be  subsequently  connected  by  a  line,  being  made 
at  the  several  points  at  which  resonance  is  replaced  by  dulness  (Fig. 
115).  The  vertical  side  of  the  right-angle  triangle  thus  erected 
corresponds  to  the  line  of  the  vertebral  spines,  extending  from  a 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        275 

point  somewhat  higher  than  the  upper  level  of  effusion  flatness  to 
the  lower  limit  of  normal  pulmonary  resonance ;  the  base  coincides 
with  the  line  of  the  latter  on  the  unaffected  side:  the  hypotenuse 
is  formed  by  a  line  (sometimes  showing  a  moderate  outward  con- 
vexity) joining  the  extremities  of  the  vertical  and  base  lines.  The 
paravertebral  triangle  disappears  or  greatly  contracts  when  the 
patient  lies  upon  the  affected  side,  and  reappears  when  the  erect 
position  is  resumed;  it  is  not  demonstrable  after  the  removal  of 
the  effusion. 

Subphrenic  abscess  may  account  for  a  paravertebral  triangle  of 
dulness  on  the  opposite  side,  but  here  the  dull  area  is  low  and  broad, 
and  not  so  prone  to  be  influenced  by  posture.  In  lumbar  abscess 
Ewart  has  detected  a  similar  percussion  finding  that  gave  way  to 
normal  pulmonary  resonance  as  soon  as  the  pus  was  evacuated. 
Ascites  sometimes  produces  a  bilateral  triangle  of  paravertebral 
dulness,  differing  from  that  due  to  a  bilateral  pleural  effusion  in 
being  perfectly  symmetric,  of  greater  width,  and  of  lesser  height.  In 
abdominal  cyst  paravertebral  dulness  has  been  found  by  Smithies, 
who  also  noted  in  pregnancy  a  roughly  triangular  dull  patch,  with 
a  flat  summit  and  convex  hypotenuse,  to  the  left  of  the  spine. 

Auscultation. — Partial  or  complete  suppression  of  the  respiratory 
murmur  is  the  rule  below  the  upper  limit  of  the  effusion,  above  which 
loud  bronchovesicular  or  bronchial  breathing  is  produced  by  the  com- 
pressed lung.  On  the  unaffected  side  there  is  a  compensatory  exag- 
geration in  the  intensity  of  the  breath-sounds.  Exceptionally,  in 
the  case  of  extreme  pulmonary  compression  and  bronchial  occlusion 
by  a  massive  effusion,  practically  no  respiratory  sounds  are  audible 
over  the  affected  half  of  the  thorax.  In  contrast  to  this,  there  are 
certain  effusions,  occurring  especially  in  children,  over  which  distant, 
though  distinct,  tubular  or  even  amphoric  respiration  is  heard,  and 
in  the  face  of  such  findings  one  must  carefully  exclude  the  possibility 
of  a  coexisting  pulmonary  consolidation  or  cavity. 

In  general,  the  voice-sounds  are  weakened  or  quite  obliterated  by  an 
effusion,  save  in  those  cases  which  afford  bronchial  breathing  and,  in 
consequence,  a  corresponding  degree  of  bronchophony.  The  nasal 
bleating  of  egophony  is  frequently  recognized  near  the  upper  level  of 
percussion  flatness.  Baccelli's  sign  (the  transmission  of  whispering 
pectoriloquy  through  a  serous  but  not  through  a  purulent  exudate)  is 
by  no  means  distinctive;  the  whispered  voice  is  inaudible  in  many 
serofibrinous  as  well  as  purulent  effusions.  As  the  volume  of  the 
fluid  diminishes  and  the  natural  resiliency  of  the  lung  is  restored,  the 
normal  respiratory  and  voice-sounds  gradually  reappear  from  above 
downward,  both  at  the  site  of  the  effusion  and  in  the  lung  above  it. 


276  PHYSICAL   DIAGNOSIS 

During  the  first  stage  of  the  process  auscultation  over  the  dry, 
inflamed  pleura  reveals  numerous  friction-sounds  (jrictio  indux), 
like  those  of  acute  fibrinous  pleurisy,  though  generally  of  greater 
intensity  and  wider  distribution.  When  the  exudate  is  poured  out 
these  sounds,  of  course,  disappear  below  the  upper  level  of  the  fluid, 
above  which,  however,  friction  may  continue  to  be  heard,  owing  to 
patches  of  dry  pleurisy  here  coexisting.  As  the  effusion  diminishes, 
allowing  the  roughened  pleural  surfaces  again  to  rub  together  with 
respiration,  the  primary  friction-sounds  reappear,  as  thefrictio  redux, 
and  this  sign  may  stubbornly  persist  for  a  long  period  after  complete 
resorption  has  taken  place,  the  sounds  possibly  acquiring  a  coarse 
grating  or  creaking  quality  suggestive  of  extensive  pleural  roughening. 

Diagnosis. — There  is  no  difficulty  in  recognizing  a  large  effusion 
by  this  distinctive  group  of  physical  signs:  unilateral  immobility 
and  overfulness  of  the  chest,  with  absence  of  the  diaphragm  shadow; 
a  zone  of  basal  flatness  over  which  tactile  fremitus,  vocal  resonance, 
and  respiratory  sounds  are  abolished,  and  above  which  they  are 
exaggerated  and  attended  by  Skodaic  resonance;  flatness  in  Traube's 
space  and  at  one  base  a  para  vertebral  triangle  of  shifting  dulness; 
and  various  visceral  displacements. 

But  the  diagnosis  is  not  always  so  clear  as  the  above  paragraph 
implies,  for  a  moderate  pleural  effusion,  particularly  in  a  child,  may 
afford  two  most  significant  indications  of  croupous  pneumonia — 
bronchophony  and  bronchial  breathing  of  the  most  exquisitely  tubular 
type;  while,  on  the  other  hand,  there  are  certain  cases  of  massive 
pneumonia  which,  by  fault  of  bronchial  occlusion,  closely  ape  the 
auscultatory  findings  of  a  copious  effusion.  Though  in  the  doubtful 
case  the  aspirating  needle  is  usually  the  court  of  final  appeal,  it 
should  be  recalled  that  a  severe  initial  chill,  high  fever,  urgent  dyspnea, 
herpes,  rusty  sputum,  abnormal  pulse-respiration  ratio,  and  absence 
of  visceral  displacement  are  in  favor  of  pneumonia.  Another  most 
important  differential  point  is  afforded  by  percussion,  which  in 
pneumonia  shows  that  the  resiliency  appreciated  by  the  pleximeter 
finger  is  of  a  much  greater  degree  than  that  felt  in  pleural  effusion, 
the  percussion  sound  at  the  same  time  being  of  fuller  volume  and  of 
lower  pitch  over  a  consolidation. 

Should  the  diagnosis  lie  between  inflammatory  effusion  and 
hydrothorax,  it  is  to  be  recalled  that  the  latter  is  not  attended  by 
fever,  pain,  or  friction;  that  it  is  more  commonly  bilateral  than 
unilateral;  that  it  is  usually  associated  with  dropsy  of  other  parts, 
of  which  sign  some  chronic  lesion  (especially  of  the  heart  or  the 
kidneys)  is  the  obvious  factor.  Paracentesis  yields  in  hydrothorax  a 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        277 

fluid  of  lower  specific  gravity,  smaller  albumin  content,  and  less 
coagulability  than  that  due  to  an  inflammatory  exudate.  (See 
p.  53.)  Absence  of  voice  and  respiratory  sounds  and  visceral  dis- 
placements cannot  be  taken  as  criteria  of  differentiation,  being 
common  to  both  conditions;  but,  as  a  rule,  the  basal  flatness  of 
hydrothorax  is  capped  by  a  horizontal,  not  an  S-shaped,  line.  A 
point  of  some  moment  is  the  comparative  ease  with  which  movable 
flatness  is  demonstrable  in  hydrothorax,  as  contrasted  with  the  great 
difficulty,  usually  the  impossibility,  of  distinguishing  such  a  sign  in 
an  inflammatory  effusion. 

In  chronic  pleural  thickening  the  association  of  a  restricted  respira- 
tory excursion,  enfeebled  breathing,  deficient  fremitus,  and  flatness 
at  one  base  gives  a  close  imitation  of  the  physical  signs  of  an  effusion. 
But  in  thickened  pleura  the  chest-wall  is  likely  to  be  retracted  and 
the  heart  drawn  toward  the  affected  side,  while  the  opposite  lung  may 
be  in  a  state  of  permanent  overinflation;  the  flatness  often  acquires  a 
peculiarly  wooden  quality  and  lacks  a  clean-cut  marginal  definition 
and  S-curved  summit;  and  no  movable  dulness  alongside  the  spine 
can  be  mapped  out.  In  pleural  thickening,  moreover,  there  are 
generally  evidences  of  pulmonary  fibrosis  and  a  history  of  some 
primary  disease  to  account  for  the  pleural  changes. 

A  large  pericardial  effusion  may  be  distinguished  from  fluid  within 
the  left  pleural  sac  by  the  following  differences:  in  pericardial  effu- 
sion the  displacement  of  the  heart  is  upward  rather  than  to  the 
right  of  the  sternum;  the  flatness  is  roughly  pyramidal  in  shape 
and  corresponds  to  the  outline  of  the  distended  pericardium,  while 
immediately  to  the  left,  and  perhaps  also  in  the  axilla,  the  percus- 
sion sound  is  Skodaic.  Pulmonary  resonance,  rather  than  movable 
dulness,  is  found  at  the  base  posteriorly.  Other  signs  pointing  to 
pericardial  effusion  include  apical  weakness  and  basal  intensity  of 
the  cardiac  sounds,  a  feeble  and  sometimes  paradoxic  pulse,  and 
the  existence  of  dyspnea  of  a  most  extreme  grade. 

Enlargement  of  the  hepatic  area,  as  from  abscess,  cancer,  or  echino- 
coccus  of  the  right  lobe,  may  account  for  a  basal  zone  of  flatness,  with 
abolished  fremitus  and  respiratory  sounds,  thereby  suggesting  a 
right-sided  pleural  effusion.  But  in  these  conditions  the  upper 
limit  of  flatness  is  likely  to  be  horizontal,  convex,  or  irregular  (not 
S-shaped),  the  overlying  lung  does  not  emit  Skodaic  resonance,  and 
the  opposite  posterior  base  fails  to  show  a  typical  Grocco's  triangle. 
If  perihepatitis  exists,  it  is  not  unusual  also  to  hear  a  basal  friction- 
sound  below  the  upper  boundary  of  the  flatness,  while  in  echinococcus 
disease  it  may  be  possible  to  elicit  a  distinctive  hydatid  fremitus. 


278  PHYSICAL   DIAGNOSIS 

Intrathoracic  tumors  may  enfeeble  fremitus  and  respiratory  sounds, 
displace  the  heart,  and  dull  pulmonary  resonance  so  as  to  counterfeit 
a  pleural  effusion,  except  that  their  physical  signs  are  not  affected 
by  postural  changes,  are  not  uncommonly  bilateral,  and  are  generally 
limited  to  the  upper  or  middle  thorax,  being,  therefore,  underlaid 
by  a  strip  of  pulmonary  resonance  at  the  base.  If  the  neoplasm  be 
mediastinal,  the  signs  are  usually  parasternal  and  attended  by 
characteristic  evidences  of  intrathoracic  compression  affecting  the 
bronchi,  esophagus,  and  great  vessels  and  nerves  of  the  mediastinum. 
The  fact  that  tumors  of  the  lungs  and  pleura  are  prone  to  excite  a 
pleural  effusion  makes  their  recognition  possible,  in  such  instances, 
only  after  a  careful  analysis  of  the  case-history  and  the  diagnostic 
use  of  the  aspirator. 

PURULENT  PLEURISY  (Empyemaj  Pyothorax) 

Clinical  Pathology. — Empyema,  or  purulent  pleurisy,  is  generally 
secondary  to  some  preexisting  focus  of  infection,  but  exceptionally  it 
is  of  primary  origin,  especially  in  children.  The  effusion  may  be  puru- 
lent from  the  beginning,  or  the  suppuration  may  be  due  to  the  contam- 
ination of  a  serofibrinous  effusion  (rarely,  a  dry,  fibrinous  pleurisy) 
by  the  bacteria  of  suppuration.  In  children  pneumococcus  infec- 
tion, primary  or  metapneumonic,  is  the  most  active  factor  of  puru- 
lent effusions,  while  in  adults  the  streptococcus,  pneumococcus, 
and  tubercle  bacillus,  in  this  order  of  frequency,  are  the  most 
common  exciting  causes  (W.  Watson  Cheyne).  Pneumococcus 
empyemas  are  more  prone  to  spontaneous  absorption  than  those 
due  to  other  bacteria,  with  the  possible  exception  of  the  bacillus  of 
Eberth,  as  noted  by  Gerhardt,  while  purulent  effusions  referable 
to  mixed  infections  are  usually  of  graver  character  than  those  pro- 
voked by  a  single  variety  of  microorganism.  In  establishing  the 
origin  of  an  empyema  these  factors  should  be  rehearsed :  pneumonia, 
tuberculosis,  and  other  infectious  processes  of  the  lungs;  infection  by 
way  of  the  blood-  and  lymph-vessels,  as  in  the  specific  infections  and 
in  local  lesions  not  directly  contiguous  to  the  pleurae;  and  infection 
by  erosive  and  gangrenous  processes  of  the  esophagus,  stomach,  liver, 
ribs,  and  vertebrae.  Septic  wounds  of  the  chest  account  for  some 
cases  of  empyema,  which  also  can  arise  as  a  consequence  of  faulty 
asepsis  during  paracentesis. 

The  pathologic  changes  of  empyema  differ  chiefly  in  degree  from 
those  of  non-suppurative  pleurisy,  than  which  the  former  works  the 
more  serious  damage.  The  character  of  the  effusion  is  exceedingly 
variable,  ranging  from  a  thin,  moderately  opaque  seropurulent  liquid 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        279 

of  yellowish-green  hue  to  a  thick,  creamy,  yellow  pus,  the  former 
separating  on  standing  into  a  thin  zone  of  leukocytes  overlaid  by  a 
considerable  quantity  of  clear  serum,  and  the  latter  being  of  homo- 
geneous consistence.  In  fetid  cases  the  exudate  emits  a  most  offensive 
stench,  and  may  have  a  brownish  color.  Fibrin,  in  the  form  of  flakes 
or  larger  masses,  is  distributed  through  an  empyematous  effusion 
in  variable  amounts,  the  exudate  in  some  cases  being  of  a  most  decided 
fibrinopurulent  nature.  Microscopically,  leukocytes  are  the  most 
important  constituent  of  the  exudate,  whose  degree  of  purulence  is 
proportionate  to  its  richness  in  these  cells;  a  variable  number  of 
erythrocytes,  degenerate  endothelium,  fat-globules,  and  cholestenn 
crystals  are  also  found,  together  with  one  or  more  of  the  varieties 
of  bacteria  mentioned  above. 

The  pleural  surfaces  are  actively  inflamed  and  thickened  by  newly 
proliferated  vascular  connective  tissue  and  by  extensive  leukocytic 
infiltration;  they  are  covered  with  a  dense,  friable,  grayish -yellow 
pseudomembrane  or  with  a  granulating  pyogenic  membrane;  and 
sometimes  show  circumscribed  areas,  single  or  multiple,  of  necrosis. 
Through  such  breaches  in  the  integrity  of  the  pleura  the  pus 
spreads  to  other  parts,  whence  it  may,  by  the  erosion  of  fistulous 
channels,  find  spontaneous  evacuation — empyema  necessitatis.  The 
formation  of  a  fistula  between  the  pleura  and  a  bronchus  means 
the  establishment  of  a  pyopneumo thorax ;  in  other  instances  the  pul- 
monary parenchyma  becomes  the  seat  of  abscess  or  of  extensive 
gangrenous  destruction,  these  changes  being  especially  prone  to 
supervene  in  virulent  putrid  empyemas.  Fistulation  through  an 
intercostal  space,  with  discharge  of  the  pus  through  the  chest-wall, 
is  also  a  common  method  of  spontaneous  evacuation.  Less  fre- 
quently the  pus  burrows  into  the  esophagus,  the  stomach,  the  peri- 
cardium, the  opposite  pleura,  the  peritoneum,  or  even  into  such  remote 
parts  as  the  kidney,  the  lumbar  region,  and  the  groin,  but  only  in 
most  exceptional  cases  has  this  been  observed. 

Pulsating  pleurisy,  in  which  pulsations  synchronous  with  the  sys- 
tolic impulse  of  the  heart  are  palpable  and  generally  visible  in  the 
intercostal  spaces,  particularly  of  the  upper  left  chest,  is  a  rare  physical 
sign  in  pleural  effusion.  (See  Fig.  125,  p.  321.)  It  is  met  with 
especially  in  empyema  (pulsating  empyema),  both  as  a  true  intra- 
pleural  pulsation  and  as  a  throbbing  tumor  in  empyema  necessitatis; 
it  is  seen  exceptionally  in  non-purulent  effusions,  and  occasionally  it 
is  found  in  connection  with  a  coexisting  pneumothorax. 

The  mechanism  of  pulsating  pleurisy  has  long  been  a  moot  point. 
Calvert  logically  explains  the  phenomenon  by  showing  that  the  pleural 


280  PHYSICAL    DIAGNOSIS 

wall,  distended  by  fluid  and  bordering  upon  a  collapsed  lung,  lies 
in  close  contact  with  the  thoracic  aorta  whose  systolic  expansions 
are  taken  up  by  the  pleural  wall  and  thereby  transmitted  to  its  weak- 
est portion.  If  this  happens  to  be  external,  its  rhythmic  stretching 
with  each  increment  of  pressure  produces  visible  pulsations,  syn- 
chronous with  cardiac  systole,  upon  the  overlying  surface  of  the  chest. 

The  visceral  displacements  occurring  in  empyema  are  similar  to 
those  of  a  serofibrinous  effusion,  but  they  are  usually  more  striking, 
owing  to  the  greater  weight  of  the  purulent  liquid;  this  factor  plus 
the  soft,  relaxed  state  of  the  parietal  structures  around  an  empyema 
accounts  for  a  relatively  greater  depression  of  the  diaphragm  and 
a  more  decided  distention  of  the  thoracic  wall  in  this  form  of  pleural 
effusion. 

After  the  removal  of  the  exudate,  either  instrumentally  or  spon- 
taneously by  absorption  or  by  evacuation,  the  pleural  surfaces  con- 
tinue to  produce  pus  for  a  protracted  period,  and  when  this  finally 
ceases,  they  are  left  irreparably  injured.  The  damage  is  moderate 
in  some  cases,  but  in  others  there  is  inordinate  pleural  thickening 
with  extensive  pulmonary  fibrosis,  ultimately  leading  to  contraction 
of  the  lung  and  to  deformity  of  the  affected  side.  (See  Fig.  38.) 

Physical  Signs. — The  physical  signs  of  empyema  do  not  differ 
materially  from  those  of  serofibrinous  pleurisy,  in  so  far  as  palpation, 
percussion,  and  auscultation  are  concerned,  the  findings  afforded 
by  these  methods  of  research  being  identical,  whether  the  effusion 
consists  of  serum  or  of  pus.  But  inspection,  at  least  in  certain 
instances,  furnishes  signs  of  sufficient  distinction  to  warrant  separate 
mention,  in  view  of  the  difficulty  in  discriminating  between  these 
two  types  of  effusion,  without  resort  to  the  aspirating  needle. 

In  a  severe  case  the  dyspnea  is  most  striking,  and  the  patient's 
appearance  betokens  grave  sepsis — anemic  pallor,  a  hectic  flush, 
sordes,  mental  apathy,  low  delirium,  great  prostration  and  emacia- 
tion, remittent  fever,  and  recurrent  drenching  sweats.  The  enlarge- 
ment of  the  affected  side  of  the  thorax  is  generally  more  noticeable 
than  in  an  ordinary  serofibrinous  effusion,  and  the  interspaces, 
instead  of  being  merely  obliterated,  may  even  bulge  outward  between 
the  ribs.  Unilateral  enlargement  of  the  chest  is  common  in 
children,  owing  to  resiliency  of  the  thorax,  but  this  is  not 
perceptible  in  adults,  because  of  the  rigidity  of  the  mature  thorax. 
The  tissues  of  the  chest-wall  are  sometimes  boggy  and  edematous, 
and  there  may  be  either  a  discolored  local  area  of  distinct  fluctuation 
that  betrays  the  prefistulous  stage  of  an  empyema  necessitatis,  or, 
indeed,  the  fistula  itself.  The  cardiac  and  the  hepatic  displacements 


DISEASES    OF    THE    BEONCHOPULMONARY    SYSTEM        28 1 

are  likely  to  be  more  conspicuous  than  in  serofibrinous  cases,  and 
the  excessive  weight  of  a  copious  empyema  is  capable  of  depressing 
and  pushing  forward  the  diaphragm  to  such  an  extent  as  to  produce 
a  well-marked  tumor  in  the  hypochondrium  of  the  affected  side. 
As  a  rule,  Grocco's  sign  is  strikingly  shown  in  purulent  effusions, 
and  tubular  breathing,  rather  than  respiratory  silence,  is  more  com- 
mon than  in  serofibrinous  pleurisy. 

In  the  vast  majority  of  instances  the  differentiation  of  empyema 
and  the  other  forms  of  pleural  effusion  can  be  made  only  by  explora- 
tory puncture,  for  which  no  other  method  of  physical  diagnosis  is 
a  satisfactory  substitute. 

Pulsating  pleurisy  may,  at  first  glance,  suggest  aneurism  of 
the  aortic  arch,  but  in  the  former  the  pulsations  lie  far  outside  the 
course  of  the  aorta — between  the  third  and  fifth  interspaces  on  the 
anterior  or  lateral  surface  of  the  thorax,  almost  invariably  on  the  left 
side,  and  exceptionally  behind;  moreover,  the  thrill,  bruit,  cardio- 
vascular changes,  and  pressure  symptoms  of  aneurism  are  wanting. 

CIRCUMSCRIBED  PLEURISY 

Aside  from  the  local  dry  pleurisies  and  the  free  effusions  just 
discussed,  there  are  other  pleuritides  restricted  to  certain  local  areas 
of  the  pleural  sac  and  which,  because  of  this  peculiarity,  present 
physical  signs  difficult  to  appreciate  and  to  interpret.  Of  these 
circumscribed  types  of  pleuritis,  the  diaphragmatic,  the  encapsulated, 
and  the  interlobar  deserve  special  consideration. 

Diaphragmatic  Pleurisy. — This  type  of  pleural  inflammation, 
implicating  the  pleural  investments  of  the  diaphragm  and  the  lower 
pulmonary  surface,  is  commonly  attended  by  a  serofibrinous  effusion, 
though  rarely  the  exudate  is  purulent,  and  exceptionally  the  process 
consists  of  a  fibrinous  or  plastic  inflammation.  The  condition  is 
by  no  means  of  frequent  incidence,  in  comparison  with  the  ordinary 
forms  of  pleural  effusion. 

The  physical  signs  of  diaphragmatic  pleurisy  are  usually  over- 
shadowed by  the  subjective  symptoms,  in  view  of  which  the  diagnosis 
must  rest  chiefly  upon  the  symptomatology  of  the  onset  and  upon 
the  character  of  the  intense  pain  that  monopolizes  the  clinical  picture. 
The  onset,  which  is  most  likely  to  be  sudden,  may  begin  with  a  chill, 
considerable  fever,  dyspnea,  and  perhaps  vomiting.  The  pain, 
largely  due  to  phrenic  irritation  or  neuritis,  is  referred  to  the  lower 
thoracic  and  the  upper  abdominal  regions,  particularly  to  the  hypo- 
chondrium and  epigastrium.  Exquisite  tenderness  is  elicited  by 
pressure  over  the  line  of  the  diaphragm  between  the  end  of  the  tenth 


282  PHYSICAL   DIAGNOSIS 

rib  and  the  ensiform  cartilage,  and  also  along  the  course  of  the 
phrenic  nerve  in  the  supraclavicular  space  at  the  outer  border  of  the 
sternocleidomastoid  muscle  and  often  in  the  intercostal  spaces  at 
the  sternal  border.  The  pain  is  naturally  much  aggravated  by  the 
movements  of  respiration,  and  by  the  hiccough  and  vomiting  that 
prove  such  distressing  symptoms  in  many  cases.  The  abdomen, 
though  not  distended,  is  acutely  sensitive  and  resistant,  especially 
on  the  side  of  the  pleurisy. 

Owing  to  the  great  pain  the  respiratory  excursion  is  restricted  and 
the  breath-sounds  are  suppressed  on  the  affected  side,  upper  thoracic 
respiration  being  a  conspicuous  sign  on  inspection.  Exceptionally, 
dry  friction-rubs  are  audible  in  the  region  of  the  diaphragm,  and  if 
there  be  a  fairly  large  effusion,  a  basal  zone  of  flatness,  with  more  or 
less  depression  of  the  liver  or  the  spleen,  may  also  be  made  out.  Such 
visceral  displacements  are  particularly  prone  to  occur  if-  the  effusion 
be  purulent,  and  in  such  an  event  one  should  look  for  edema  of  the 
chest-wall  and  for  bulging  of  the  lower  interspaces. 

Because  of  its  violent  onset,  decided  constitutional  disturbances, 
and  active  abdominal  symptoms,  diaphragmatic  pleurisy  must  be 
carefully  distinguished  from  certain  forms  of  the  "acute  abdomen," 
notably  those  due  to  gall-stone  colic,  to  appendicitis,  and  to  acute 
peritonitis,  and  in  making  this  discrimination  due  weight  must  be 
given  to  the  clinical  history  of  the  case  in  question.  This  having 
been  analyzed,  one  may  also  succeed  in  detecting  the  basal  friction, 
the  typical  areas  of  tenderness,  and  the  unduly  striking  dyspnea, 
which  together  point  surely  to  diaphragmatic  pleural  ioflammation. 

Encapsulated  or  Encysted  Pleurisy. — In  this  variety  of  effusion, 
which  is  more  commonly  purulent  than  serofibrinous,  the  exudate, 
instead  of  being  free  in  the  pleural  cavity,  is  limited  by  inflammatory 
adhesions  to  circumscribed  areas,  the  fluid  being  thus  walled  off  into 
a  single  encapsulated  collection  or  into  several  pockets,  either  dis- 
tinct and  separate  or  communicating.  The  aspirating  needle  is  the 
only  certain  means  of  detecting  effusions  of  this  sort,  though  their 
existence  is  suggested  by  the  discovery  of  circumscribed  physical 
signs  of  fluid. 

Interlobar  Pleurisy. — This  term  is  applied  to  a  type  of  local  pleurisy 
in  which  the  exudate,  poured  out  by  the  inflamed  pleural  reflections 
between  the  lobes  of  the  lungs,  is  confined  by  adhesions  to  the  inter- 
lobar  surfaces.  A  circumscribed  exudate  of  this  sort,  which  may  be 
either  purulent  or  serofibrinous,  is  commonly  limited  to  the  septum 
between  the  right  upper  and  middle  lobes,  and,  like  other  forms  of 
walled-off  effusion,  usually  cannot  be  diagnosed  without  resort  to 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        283 

aspiration.  In  interlobar  empyema  the  pus  sometimes  fistulates 
into  a  neighboring  bronchial  tube,  such  an  accident  being  betrayed 
by  paroxysmal  cough  productive  of  a  variable  quantity  of  purulent 
sputum. 

The  physical  signs  of  an  interlobar  effusion  should  be  sought  for 
along  the  course  of  the  interlobar  septa,  the  findings  being  sharply 
restricted  to  these  lines  if  the  fluid  be  near  the  surface,  but  being 
well  below  them  if  the  process  be  deep.  Circumscribed  tender- 
ness, absence  of  tactile  fremitus  and  voice-sounds,  pleural  friction, 
feeble  respiration,  and  dulness  bordered  by  Skodaic  hyperreso- 
nance,  when  localized  near  the  levels  of  the  fourth  and  fifth  ribs, 
either  anterolaterally  or  posteriorly,  are  suggestive  findings  that 
the  Rontgen-ray  and  the  exploring  needle  may  clothe  with  cer- 
tainty. 

Mediastinal  Pleurisy. — Effusions  into  the  mediastinal  space  are 
of  rare  occurrence  and  ordinarily  represent  a  postpneumonic  com- 
plication, or  they  may  be  secondary  to  tuberculosis,  to  pulmonary 
abscess,  or  to  an  encysted  diaphragmatic  pleurisy.  As  a  rule,  such 
effusions  are  purulent  rather  than  serofibrinous.  The  physical 
signs  relate  conspicuously  to  mediastinal  pressure,  consisting  of  the 
sudden  onset  of  fever,  substernal  pain,  dyspnea,  and  cough,  and 
later,  as  the  oppression  becomes  aggravated,  orthopnea,  rapid 
respiration,  suffocative  cough,  dysphagia,  laryngeal  spasm,  hoarse- 
ness, aphonia,  and  extensive  congestion  of  the  surface  veins  de- 
velop. Apart  from  this  "mediastinal  syndrome,"  the  objective 
findings  are  in  no  wise  distinctive:  they  consist  of  an  abolition  of 
vocal  fremitus,  impaired  resonance,  and  absent  respiratory  sounds 
in  one  infrascapular  region,  contrasted  with  intense  percussion 
resonance,  and  perhaps  bronchial  respiration  at  the  apex  on  the 
same  side,  with  compensatory  hyper  resonance  over  the  opposite 
lung.  Aspiration  is  likely  to  fail  as  a  diagnostic  aid,  because  of  the 
depth  of  the  lesion  and  the  density  of  the  overlying  lung. 

CHRONIC  ADHESIVE  PLEURISY  (Chronic  Plastic  or  Fibrinous  Pleurisy ; 
Symphysis  Pleurae) 

Clinical  Pathology. — As  a  rule,  this  variety  of  pleurisy  is  a  sequel 
of  pleural  effusion,  beginning  as  an  organization  of  the  fibrous  deposit 
left  upon  the  pleural  surfaces  after  the  removal  of  the  fluid  exudate; 
less  commonly  it  represents  an  agglutination  and  fibrosis  of  the 
pleurae,  secondary  to  an  acute  plastic  pleurisy  or  developing  as  a  slow, 
insidious,  progressive  lesion  at  no  time  betrayed  by  active  symptoms. 
The  visceral  and  parietal  pleurae  are  unduly  thickened  and  inti- 


284  PHYSICAL   DIAGNOSIS 

mately  united  by  dense  fibrous  masses,  which,  if  there  be  sufficient 
respiratory  movement,  tend  finally  to  yield  to  the  incessant  traction, 
whereby  they  are  converted  into  tough  interpleural  cords;  or  the 
dcatricial  overgrowth  may  weld  the  two  pleural  membranes  into  a 
single  fibrocalcareous  layer,  sometimes  so  extensive  as  practically  to 
obliterate  the  pleural  cavity,  especially  if  the  corresponding  lung  be 
also  diseased.  In  some  instances  there  are  small  intrapleural  loculi 
of  fluid,  in  others  traction  bronchiectases  develop,  and  in  still  others 
the  lung  becomes  encapsulated  by  a  rigid,  contracting  pleural  invest- 
ment. In  consequence  of  the  pleural  lesions  the  excursion  of  the 
lung  is  limited  and  its  function  hampered;  the  pulmonary  tissue 
undergoes  extensive  compression  and  fibrosis,  the  septa  are  pene- 
trated by  fibrous  bands,  interlobar  agglutination  may  unite  two  or 
more  lobes,  and  firm  adhesions  commonly  develop,  particularly 
at  the  bases  and  at  the  apices  posteriorly.  Exceptionally,  chronic 
adhesive  pericarditis  and  proliferative  peritonitis  coexist. 

Physical  Signs. — Inspection. — In  the  average  case  one  finds 
little  else  than  a  moderate  degree  of  dyspnea,  with  slightly  impaired 
mobility  of  the  chest  on  the  affected  side,  and  not  infrequently  even 
such  clues  are  wanting.  But  when  the  pleurae  are  extensively  impli- 
cated, the  dyspnea  becomes  most  striking,  the  respiratory  movements 
are  greatly  hampered,  the  affected  side  expands  but  little,  if  at  all,  and 
may  show  a  circumscribed  area  of  flattening  or  retraction.  (See  Fig. 
45,  p.  91.)  In  cases  following  empyema  the  scar  of  the  fistulous  drain 
at  once  arrests  the  examiner's  attention,  and  it  is  in  examples  of 
this  kind  that  local  deformities  of  the  thorax,  with  drooping  of  the 
shoulder,  overlapping  of  the  ribs,  and  spinal  deflection,  become  most 
conspicuous.  (See  Fig.  38,  p.  88.)  The  heart  may  be  drawn  to  the 
right  or  to  the  left,  according  to  whether  the  traction  is  exerted  by 
right-  or  by  left-sided  adhesions,  and  in  old  unilateral  lesions  com- 
pensatory enlargement  of  the  opposite  half  of  the  chest  tends  to 
supervene.  Apical  adhesions  that  irritate  the  first  thoracic  sympa- 
thetic ganglion  are  betrayed  by  unilateral  sweating  or  flushing  of  the 
face  and  by  dilatation  of  the  pupil.  Evidences  of  venous  stasis, 
from  dilatation  of  the  right  heart,  may  appear  late,  in  cases  of  great 
chronicity,  and  in  such  instances  one  commonly  observes  a  network 
of  delicate  venous  radicles  curving  across  the  lower  anterior  thorax. 

Palpation. — The  intensity  of  tactile  fremitus  varies  with  the 
peculiarities  of  the  lesion  in  the  individual  case:  it  is  ordinarily 
enfeebled  or  abolished  over  areas  of  simple  pleural  thickening,  but 
despite  this  barrier  to  voice  vibrations,  the  fremitus  may  be  clearly 
conducted  to  the  surface  by  bands  of  compact  pleuropulmonary 
adhesions.  Friction  fremitus,  of  a  coarse,  grating  quality,  is  appre- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        285 

ciable  over  patches  of  mobile  pleural  roughening.  In  moderately 
advanced  cases  the  hand  is  more  useful  than  the  eye  in  detecting 
respiratory  immobility,  particularly  circumscribed,  of  the  chest-wall. 

Percussion. — The  thicker  the  pleurae  and  the  greater  the  pulmonary 
fibrosis,  the  less  resonant  the  percussion  sound  over  the  parts  affected. 
Resonance  may  be  simply  impaired,  as  shown  by  a  slightly  elevated 
pitch,  shortened  duration,  and  increased  resistance;  or  there  may 
be  dulness  of  a  peculiar  wooden  character,  with  most  striking  resist- 
ance to  the  pleximeter  finger.  Emphysematous  percussion  sounds 
over  the  opposite  lung  are  familiar  findings  in  advanced  cases. 

Auscultation. — The  respiratory  murmur  and  vocal  resonance  are 
enfeebled,  especially  at  the  base,  in  proportion  to  the  degree  of  pleural 
thickening,  of  respiratory  restriction,  and  of  vesicular  obliteration. 
Aside  from  these  findings,  many  cases  show  the  auscultatory  changes 
of  such  coexisting  processes  as  pulmonary  fibrosis  and  emphysema, 
bronchitis,  and  bronchiectasis  (q.  v.).  Friction,  if  audible,  is  gen- 
erally loud,  leathery,  and  creaking. 

Diagnosis. — The  association  of  thoracic  deformity  and  immo- 
bility with  such  signs  as  enfeebled  breathing,  diminished  tactile 
fremitus,  wooden  dulness,  and  coarse  friction  makes  a  well-developed 
adhesive  pleurisy  an  easily  recognized  condition.  In  doubtful  cases, 
presenting  a  less  clear-cut  symptomatology,  the  patient's  history  and 
the  careful  study  of  the  respiratory  murmur  and  the  percussion  find- 
ings are  to  be  relied  upon  as  the  chief  diagnostic  clues. 

HYDROTHORAX  (Pleural  Dropsy) 

Hydrothorax,  or  dropsy  of  the  pleural  cavity,  is  usually  part  and 
parcel  of  an  anasarca  due  to  chronic  cardiac,  renal,  or  hepatic  dis- 
ease or  to  high-grade  anemia.  The  effused  fluid  is  a  simple  clear 
transudate,  of  lemon-yellow  color,  poor  in  cellular  elements,  and  con- 
taining little  or  no  fibrin;  the  specific  gravity  rarely  exceeds  1015,  the  al- 
bumin content  is  not  more  than  20  or  30  grams,  and  the  formed  elements 
are  chiefly  endothelial  cells  shed  by  the  pleural  surfaces.  (See  p.  53.) 
Here  may  be  noted  Peju's  observation,  that  pleural  dropsies  occurring 
in  subjects  of  anthracosis  may  consist  of  thin  black  fluid  charged 
with  carbon  particles.  Hydrothorax  is  generally  bilateral,  though 
unilateral  effusions  are  also  met  with,  chiefly  in  connection  with 
chronic  cardiac  disease,  in  which  right-sided  hydrothorax,  frequently 
preceding  a  general  edema,  is  the  rule,  probably  because  of  pressure 
on  the  vena  azygos  major  by  an  enlarged  right  auricle  (Baccelli). 
When  stasis  thus  provoked  extends  to  the  vena  azygos  minor,  effusion 
into  the  left  pleural  sac  occurs,  and  in  this  manner  a  bilateral  hydro- 
thorax  is  established,  the  volume  of  which  is  usually  greater  on  the  right 


286  PHYSICAL    DIAGNOSIS 

side.  Pressure  by  the  dilated  heart  upon  the  pulmonary  veins  is  the 
explanation  of  cardiac  hydrothorax  given  by  Fetterolf  and  Landis. 
In  certain  cases  of  Laennec's  cirrhosis  there  is  also  a  tendency  toward 
right-sided  hydrothorax,  attributable,  at  least  in  part,  to  azygos 
compression  by  the  enlarged  veins  of  the  esophageal  plexus  (Martini) . 
Unilateral  hydrothorax  may  be  associated  with  local  lesions  of  the 
same  side  (neoplasm,  fibrosis,  aneurism)  that  compress  the  great 
vessels  at  the  pulmonary  radix;  it  sometimes  affects  the  free  pleural 
sac  opposite  the  one  obliterated  by  universal  adhesions;  it  occurs 
rarely  (as  "  hydrops  ex  vacuo")  in  the  pleuropulmonary  space  created 
by  the  recession  of  a  tightly  contracted  lung;  and  it  may  exist  as  a 
loculated  collection  of  fluid  walled  off  by  impermeable  adhesions. 
In  pure  hydrothorax  the  pleural  surfaces  are  not  inflamed,  though 
this  change  tends  to  supervene  as  the  result  of  the  chronic  conges- 
tion, and  the  primary  transudate,  in  such  an  event,  acquires  many 
of  the  characteristics  of  an  inflammatory  exudate. 

The  physical  signs  are  those  of  intrapleural  fluid,  generally  bilateral, 
unattended  by  pain  and  friction,  and  associated  with  clear  evi- 
dences of  the  underlying  disease.  Dyspnea  and  cough  in  a  dropsical 
subject  should  always  prompt  a  search  for  fluid  within  the  pleural 
sacs.  The  differences  between  the  physical  signs  of  hydrothorax 
and  an  inflammatory  pleural  effusion  have  been  described  under 
the  latter.  (See  p.  276.) 

HEMOTHORAX    (Pleural  Hemorrhage) 

Hemothorax,  or  hemorrhage  into  the  pleural  cavity,  results  from 
accidents  such  as  traumatism  of  the  chest,  rupture  of  an  aneurism, 
erosion  of  a  blood-vessel,  and  free  vascular  oozing  incident  to  the 
hemorrhagic  diathesis.  The  extravasated  blood  coagulates,  the 
serum  is  rapidly  absorbed,  and  the  clot  is  deposited  upon  the  most 
dependent  surface  of  the  pleura,  whence,  if  uninfected,  it  is  even- 
tually removed  by  absorption,  without  giving  rise  to  pleural  inflam- 
mation. Infection,  however,  is  not  unlikely  to  take  place,  partic- 
ularly in  hemothorax  due  to  wounds  of  the  chest-wall  or  secondary 
to  some  erosive  lesion  that  establishes  a  fistulous  communication 
with  the  gullet  or  the  larger  air-passages,  and  in  such  cases  the  prompt 
onset  of  a  purulent  pleurisy  is  to  be  expected.  ' 

The  physical  signs  relate  to  a  rapidly  accumulating  pleural  effusion, 
with  or  without  evidences  of  actual  pleuritis.  These  findings,  cor- 
related with  the  patient's  clinical  history  and  with  the  objective 
symptoms  of  acute  hemorrhage  and  shock,  are  generally  sufficient 
to  warrant  the  diagnosis  of  hemorrhage  into  the  pleural  cavity. 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        287 

CHYLOTHORAX  (Hydrops  Chylos«s) 

Chylothorax,  or  the  presence  of  an  effusion  of  chyle  in  the  pleural 
sac,  is  a  very  rare  affection,  arising  in  consequence  of  a  leakage  of 
chyle  from  the  thoracic  duct  or  from  a  large  intrathoracic  lymphatic 
trunk.  This  accident  may  be  of  traumatic  origin,  or  may  be  due 
to  cancerous  erosion,  to  lesions  of  the  lymph-vessels,  or  to  left  sub- 
clavian  venous  thrombosis;  rarely,  it  has  been  ascribed  to  filariasis. 
The  effused  fluid  consists  of  a  turbid,  creamy  emulsion  of  fat, 
having  either  a  faintly  sweetish  odor  or  none  at  all,  being  peculiarly 
resistant  to  decomposition,  and  clearing  on  shaking  with  ether,  but 
not  doing  so  on  centrifugalization.  The  specific  gravity  of  the 
transudate  ordinarily  ranges  between  1015  and  1020,  and  it  contains 
approximately  from  3  per  cent,  of  albumin  to  twice  this  amount 
or  more,  together  with  a  variable  sugar  content,  and,  inconstantly, 
fibrin  and  casein. 

The  physical  signs  of  chylothorax  are  those  of  a  pleural  effu- 
sion, either  unilateral  or  bilateral,  and  the  diagnosis  must  be 
made  by  thoracentesis.  True  chylous  hydrops,  rather  than  a  chyli- 
form  effusion,  is  indicated  by  aspirating  a  creamy  fluid  yielding  at 
least  0.2  per  cent,  of  sugar,  abundantly  charged  with  very  minute 
fat-droplets,  and  containing  relatively  few  cellular  elements.  In 
contrast,  a  chyliform  effusion  shows  a  lower  sugar  content,  fewer 
and  larger  fat-particles,  and  a  greater  number  of  degenerate  cells. 
When  both  types  of  effusion  coexist,  as  is  sometimes  the  case, 
examination  of  the  fluid  is  obviously  of  no  avail,  and  in  this  con- 
tingency the  differentiation,  if  one  can  be  made,  must  needs  rest 
largely  upon  the  case  history.  Chylothorax  is  suggested  when  it  is 
possible  to  identify  some  factor  of  chyle  leakage:  trauma,  cancer 
of  the  pleura,  thrombosis  of  the  left  subclavian  vein,  or,  possibly, 
filarial  infection;  while  chyliform  effusions,  though  also  met  with 
in  pleural  cancer,  are  likely  to  be  associated  with  severe  anemias, 
tuberculosis,  chronic  cardiac  disease,  and  grave  cachectic  states. 
(C/.  Chyliform  Pleurisy,  p.  269.) 

PNEUMOTHORAX  (Hydropneumothorax;   Pyopneumothorax;    Hemo- 

pneumo  thorax) 

Clinical  Pathology. — Pneumothorax,  or  the  accumulation  of  air 
within  the  pleural  cavity,  is  generally  attended  by  an  effusion  of 
serum,  pus,  or,  rarely,  blood,  and  hence  the  more  specific  terms, 
hydropneumothorax,  pyopneumothorax,  and  hemopneumothorax  are 
appropriate,  according  to  the  character  of  the  fluid. 


288  PHYSICAL   DIAGNOSIS 

Owing  to  the  elastic  tension  of  the  lungs,  the  normal  pressure 
within  the  pleural  cavity  (754  mm.  of  Hg)  is  about  6  mm.  lower 
than  that  of  the  pulmonary  vesicles  and  air-passages  (760  mm.  of 
Hg.),  and  in  consequence  of  this  difference,  designated  as  "negative 
intrapleural  pressure,"  the  lungs  are  kept  in  close  contact  with  the 
inner  thoracic  wall  and  the  two  pleural  surfaces  are  intimately  approxi- 
mated. So  soon,  however,  as  a  communication  is  established 
between  the  atmospheric  air  and  the  pleural  sac,  the  latter  sucks 
in  sufficient  air  to  satisfy  its  negative  pressure,  or,  in  other  words,  to 
equalize  the  intrapleural  and  the  intrapulmonary  pressures.  In 
consequence,  the  lung,  by  virtue  of  its  inherent  elasticity,  immediately 
recoils  from  the  chest-wall  and  contracts,  for  its  so  doing  is  not  now 
prevented  by  a  high  intrapulmonary  tension,  and  the  pleural  cavity, 
whose  membranes  are  no  longer  opposed,  is  widely  distended  by 
the  aspirated  atmospheric  air.  This  constitutes  pneumothorax. 
That  pneumothorax  does  not  invariably  follow  pleurotomy  is  due  to 
increased  pressure,  referable  to  strong  respiratory  efforts,  within  the 
corresponding  lung,  whereby  its  contractility  is  overcome  and  the 
organ  becomes  overdistended.  This  not  only  insures  adequate 
approximation  of  the  two  pleural  surfaces,  but  may  even  cause  pro- 
trusion of  the  lung  through  the  breach  in  the  chest-wall,  and  thus 
produce  a  pulmonary  hernia. 

Air  enters  and  accumulates  within  the  pleural  cavity  in  conse- 
quence of  numerous  different  factors,  of  which  pulmonary  tuberculosis 
is  by  all  odds  the  most  common.  Fully  90  per  cent,  of  all  pneumo- 
thoraces  are  due  to  this  cause  (Weil;  West;  Walsh),  the  entrance 
of  air  usually  being  through  a  breach  made  in  the  pleura  by  a  small 
interpleural  or  subpleural  tubercle,  or,  less  frequently,  through  the 
rupture  of  a  pulmonary  cavity  lying  immediately  beneath  the  pleura. 
The  favorite  site  of  such  perforations  is  toward  the  base  rather  than 
the  apex  of  an  upper  lobe,  especially  on  the  left  side.  Empyema 
is  also  an  important  cause  of  pneumothorax,  and  in  this  disease 
the  air  commonly  gains  access  through  a  bronchopleural  sinus, 
while  only  exceptionally  does  it  enter  by  the  fistulous  tract  in  the 
chest-wall  created  by  an  empyema  necessitatis.  Other  destructive 
diseases  that  may  produce  pneumothorax,  by  the  erosion  of  a  fistula 
into  the  lung  and  bronchial  tubes,  include  abscess,  gangrene,  cancer, 
and  hydatid  cyst  of  the  lung,  suppurative  tracheobronchial  adenitis, 
and  bronchiectasis;  while  in  certain  instances  the  condition  is  refer- 
able primarily  to  esophageal  erosion,  to  similar  disease  of  the  parietal 
structures,  and  to  ulcerative  lesions  beginning  in  a  subphrenic 
viscus  (stomach,  liver,  intestine)  and  ultimately  perforating  the 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        289 

pleura,  as  a  rule,  after  first  invading  the  corresponding  lung.  Pneu- 
mothorax  has  been  known  to  follow  violent  respiratory  effort  and 
severe  muscular  strain,  the  stress  of  which  is  sometimes  sufficient 
to  rupture  even  a  healthy  lung,  though  more  often  a  lung  thus  torn 
is  found  to  be  the  seat  of  latent  tuberculosis,  emphysematous  bullae, 
infarction,  or  some  other  lesion  that  weakens  its  texture.  Violent 
contusions  and  penetrating  wounds  of  the  chest-wall  also  account 
for  the  entrance  of  air  into  the  pleural  sac,  and  to  the  latter  so-called 
traumatic  type  of  pneumothorax  the  bungling  use  of  the  aspirating 
needle  occasionally  contributes  a  case.  In  an  exceptional  instance 
the  pleural  cavity  fills  with  gas  evolved  by  the  B.  aerogenes  capsulatus 
growing  in  a  pleural  exudate. 

Save  for  rare  exceptions,  the  disease  is  unilateral,  and  the  collec- 
tion of  air  fills  and  thoroughly  permeates  the  free  space  within  one 
pleural  sac — general  or  complete  pneumothorax;  occasionally,  the  air 
is  circumscribed,  by  air-tight  adhesions,  to  a  part  of  the  pleural  cav- 
ity— circumscribed  or  limited  pneumothorax:  simultaneous  distention 
of  both  pleural  spaces,  or  bilateral  pneumothorax,  is  a  rare  clinical 
curiosity  in  which  the  subject's  life  is  a  matter  of  hours.  If  the 
fistulous  tract  leading  to  the  pleural  cavity  be  patent  and  permits 
the  free  passage  of  air  into  and  out  of  the  pleural  chamber,  an  open 
pneumothorax  exists,  and  in  this  variety  of  the  disease  the  intra- 
pleural  and  atmospheric  pressures  are  equal.  Should  the  orifice 
become  sealed,  as  by  adhesions  or  by  a  bit  of  lymph,  a  closed  pneu- 
mothorax is  established,  in  which  the  intrapleural  pressure  either 
remains  atmospheric  or  gradually  becomes  negative,  if  the  excess 
air  be  finally  absorbed.  An  opening  provided  with  a  valvular 
mechanism,  which  admits  air  with  inspiration,  but  prevents  its 
free  escape  with  expiration,  distinguishes  a  -valvular  or  ventilated 
pneumothorax,  a  type  associated  with  exceedingly  high  intrapleural 
tension.  Primarily,  the  great  proportion  of  all  pneumothoraces  are 
valvular,  but  the  type  of  the  disease  is  subject  to  change  from  time 
to  time,  because  of  the  readiness  with  which  structural  alterations 
in  the  fistulous  opening  take  place. 

The  immediate  effect  of  pneumothorax  is  a  great  distention  of  the 
chest  on  the  affected  side,  and  on  puncture  of  the  pleural  sac  the 
air  may  escape  with  considerable  force,  if  positive  intrapleural 
pressure  exists.  If  free,  the  lung  on  the  diseased  side  is  collapsed, 
contracted,  and  compressed,  lying  in  a  small,  carnified  mass  along 
the  vertebrae;  if  the  lung  be  bound  down  by  adhesions,  it  shrinks 
in  a  more  irregular  manner,  according  to  the  situation  of  the  bands 
of  traction.  The  mediastinum  and  its  contents,  unless  firmly 
19 


2QO  PHYSICAL   DIAGNOSIS 

anchored  by  adhesions,  are  displaced  toward  the  sound  side  by  the 
higher  pressure  in  the  pneumothoracic  pleura;  and  by  a  similar 
mechanism  the  diaphragm,  with  the  liver  and  spleen,  is  unduly 
depressed.  Pleural  effusion  is  an  almost  constant  sequel  in  subjects 
that  survive,  the  exudate  being,  in  order  of  frequency,  serofibrinous, 
purulent,  or,  exceptionally,  hemorrhagic. 

Physical  Signs. — Inspection. — The  affected  side  is  distended 
and  immobile,  the  intercostal  spaces  being  effaced  and  the  diaphragm 
shadow  abolished,  while  in  contrast  to  this  the  opposite  half  of  the 
thorax  shows  exaggerated  respiratory  movements.  The  visible 
cardiac  impulse  is  displaced  toward  the  sound  pleura,  and  the  liver 
may  bulge  outward  below  the  right  costal  margin.  Distressful 
dyspnea, .  paroxysmal  cough,  cyanosis,  rapid  feeble  pulse,  and  a 
state  of  suffocation  and  collapse  are  notable  objective  symptoms  of 
acute  general  pneumothorax,  but  in  cases  of  long  standing  the  urgency 
of  these  signs  is  greatly  modified. 

Fluoroscopic  examination  reveals  an  abnormally  clear  and  bright 
appearance  of  the  affected  side,  with  contrasting  shadows  of  carnified 
lung  above  and  of  fluid  below,  in  case  these  attendant  conditions 
be  sufficiently  developed  to  obstruct  the  passage  of  the  rays  (Fig. 
116).  The  mediastinal  shadow  lies  far  from  its  natural  site,  and 
the  diaphragm  is  depressed  and  unnaturally  immobile.  In  some 
cases  the  phrenic  vault  shows  a  downward  convexity,  and  the 
normal  inspiratory  fall  and  expiratory  rise  of  the  diaphragm  are 
reversed.  If  the  displacements  be  unusually  striking,  as  is  the 
tendency  in  valvular  pneumothorax  with  excessively  high  tension, 
practically  nothing  is  seen  with  the  fluoroscope  save  the  clean-cut 
shadows  of  the  ribs  and  clavicle  against  a  bright  background  corre- 
sponding to  the  boundaries  of  the  distended  pleural  sac. 

Palpation. — Vocal  fremitus  is  diminished  or  entirely  lost  over  the 
air-distended  pleura,  though  toward  the  apex  there  may  be  intense 
voice  vibrations  referable  to  pulmonary  compression  or  consolida- 
tion. The  liver,  in  right-sided  pneumothorax,  is  palpable  far  below 
the  costal  margin,  the  displacement  of  this  organ  being,  as  a  rule, 
much  more  conspicuous  than  in  a  simple  fluid  effusion  within  the 
pleura.  Succussion  fremitus  (v.  i.)  is  occasionally  palpable  when 
the  pleura  contains  both  air  and  fluid. 

Percussion. — Generally,  the  percussion  sound  is  unduly  loud,  sonor- 
ous, and  hyperresonant;  sometimes  it  is  dull,  muffled,  and  toneless; 
and  exceptionally  it  is  tympanitic  or  even  amphoric.  Normal  pul- 
monary resonance,  although  rare,  is  not  incompatible  with  the 
lesion  in  question.  These  differences,  which  relate  to  the  typical 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        2QI 

instance  of  general  pneumothorax,  are  determined  mainly  by 
the  degree  of  intrathoracic  pressure  existing  in  the  individual 
case,  and  the  character  of  the  percussion  sound  serves  to  index 
the  resiliency  of  the  thoracic  wall.  Thus,  despite  the  impracti- 
cability of  differentiating  the  three  forms  of  the  disease  by  per- 
cussion alone,  it  is  true  that  in  valvular  and  in  closed  pneumo- 
thorax one  expects  to  find  sonorous  hyperresonance  or  muffled 
dulness,  according  to  whether  the  pressure  be  moderate  or  extreme; 


Fig.  n6. — Radiograph  of  a  left  pneumothorax.  Posterior  aspect  showing 
shadow  of  consolidated  lung  above  the  air-distended  pleura.  (Plate  by  Dr.  W.  F. 
Manges.) 

while  in  open  pneumothorax,  where  the  intrapleural  pressure  is 
merely  atmospheric,  there  may  be  the  proper  relaxation  of  the  parietes 
to  afford  tympany.  Cracked-pot  resonance  with  Wintrich  s  sign 
may  be  elicited  over  a  pneumothorax  communicating  with  a  patu- 
lous  bronchus.  The  percussion  resistance  also  varies  with  the 
elasticity  of  the  chest- wall:  commonly,  a  sort  of  "air-cushion"  sensa- 
tion is  felt  by  the  pleximeter  finger,  but  should  the  tension  be  exces- 
sive, the  resistance  is  almost  board-like.  The  percussion  sounds, 
whatever  be  their  exact  quality,  are  readily  distinguishable  from 
those  found  over  the  opposite — and  perhaps  vicariously  hyper- 


2Q2  PHYSICAL    DIAGNOSIS 

resonant — lung,  and  their  extension  beyond  the  median  and  infe- 
rior limits  of  the  normal  pleura  is  readily  determined. 

The  coexistence  of  fluid  is  revealed  by  a  basal  zone  of  flatness 
which  readily  shifts  with  changes  in  the  subject's  posture,  this  sign 
of  movable  flatness  being  much  more  evident  and  easy  to  detect 
in  pneumothorax  with  fluid  than  in  uncomplicated  hydrothorax 
or  in  inflammatory  effusion. 

Auscultation.— Over  the  distended  pleura  the  respiratory  murmur 
is  suppressed,  often  to  the  point  of  absolute  silence;  if  at  all  audible, 
the  breathing  possesses  a  far-away  amphoric  tone  or  a  distant  bron- 
chial quality,  should  the  sound  transmission  travel  by  way  of  a 
patch  of  compressed  lung  abutting  upon  an  open  bronchial  tube. 
Vocal  resonance  is  distant  and  frequently  amphoric  and  echoing. 
Over  the  unaffected  side  the  respiratory  and  the  voice-sounds  are 
puerile  and  abnormally  loud. 

Four  noteworthy  adventitious  soiuids  should  be  sought  for  in 
pneumothorax:  the  succussion  splash  (succussio  Hippocratis)  of 
Hippocrates;  the  coin  sound  (bruit  d'airairi)  of  Trousseau;  the 
metallic  tinkle  (gutta  cadens)  of  Laennec;  and  the  pulmonary  fistula 
sound  (water-whistle  noise)  of  Riegel.  These  important  signs,  indi- 
cating both  air  and  fluid  within  the  pleural  sac,  have  been  described 
in  a  preceding  section,  and,  therefore,  require  no  further  comment 
in  this  connection.  (See  p.  165  et  seq.)  Other  abnormal  sounds, 
developed  by  the  acts  of  coughing  and  deep  respiration,  consist  of 
a  medley  of  bubbling  rales  of  ringing,  metallic  quality  and  of 
pleural,  pulmonary,  and  bronchial  origin. 

The  abnormal  situations  of  the  cardiac  and  hepatic  percussion 
areas  are  generally  well  defined,  especially  in  cases  associated  with 
excessively  high  intrapleural  pressure:  for  example,  a  valvular  pneu- 
mothorax, if  left  sided,  may  entirely  obliterate  cardiac  dulness  to  the 
left  of  the  midsternal  line,  or,  if  right  sided,  may  depress  the  liver 
so  that  its  upper  border  of  dulness  is  at,  if  not  below,  the  arch  of  the 
ribs.  To  a  less  striking  degree  the  splenic  area  is  depressed  by  the 
pressure  of  air  within  the  left  pleural  cavity.  In  left  pneumothorax 
Calvert  has  noted  that  an  apex-beat  invisible  in  recumbency  becomes 
apparent  when  the  subject  leans  forward  so  as  to  allow  the  mobile 
heart  (for  its  pulmonary  support  is  lost)  to  swing  forward  against 
the  chest-wall. 

Diagnosis. — The  sudden  onset  of  urgent  dyspnea,  cyanosis,  and 
collapse  is  a  most  significant  indication  of  acute  general  pneumo- 
thorax, particularly  if  this  syndrome  be  observed  in  a  phthisical 
subject  The  principal  confirmatory  signs  comprise  unilateral  dis- 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM         293 

tention,  immobility,  and  hyperresonance  of  the  thorax;  diminished 
or  absent  vocal  fremitus  and  resonance;  abolished  or  distantly 
amphoric  respiratory  sounds;  and  remarkable  displacement  of  the 
heart,  liver,  and  diaphragm.  If  an  effusion  also  exists,  shifting 
dulness  at  the  base  will  be  found,  as  well  as  the  peculiar  ringing  and 
metallic  sounds  so  distinctive  of  air  and  fluid  within  a  pleural  sac. 
A  circumscribed  partial  pneumothorax  may  afford  no  distinctive 
signs  whatever — the  so-called  "mute  pneumothorax"  of  Sabourin. 

Pleural  effusion,  either  exudative  or  transudative,  is  sometimes 
suggested  by  a  pneumothorax  attended  by  a  collection  of  intra- 
pLeural  fluid  of  sufficient  volume  to  cause  an  extensive  basal  area  ot 
flatness,  overlaid  by  dull  hyperresonance  and  provocative  of  con- 
siderable visceral  displacement;  the  fact  that  tubular  or  amphoric 
breathing  above  and  respiratory  silence  below  may  be  common  to 
both  conditions  makes  their  discrimination  still  more  difficult. 
In  hydropneumothorax  or  pyopneumothorax,  however,  the  thoracic 
distention  is  much  more  decided  and  the  visceral  displacements  are 
more  conspicuous  than  in  simple  effusion;  the  basal  flatness  has  a 
perfectly  horizontal  upper  level  that  readily  shifts  when  the  patient's 
position  is  altered;  and  such  important  auscultatory  findings  as 
the  succussion  sound,  metallic  tinkling,  and  the  coin  sound  are 
generally  demonstrable. 

Certain  cases  of  unilateral  emphysema,  secondary  to  wide-spread 
fibrosis  of  the  opposite  lung,  in  the  course  of  time  produce  an  enlarge- 
ment of  one-half  of  the  thorax,  which,  on  percussion,  emits  a  sound 
whose  intense  hyperresonance  is  comparable  to  that  found  in  pneumo- 
thorax, and  iii  the  face  of  such  findings  the  presence  of  dyspnea, 
cyanosis,  and  cough  makes  the  resemblance  still  closer.  But  despite 
these  similarities,  the  differentiation  is  not  difficult,  when  one  con- 
trasts the  vertical  excursions  of  the  thorax,  the  expiratory  type  of 
dyspnea,  and  the  attenuated  (though  still  vesicular)  respiratory 
murmur  of  emphysema  with  the  thoracic  immobility,  the  desperate 
suffocation,  and  the  respiratory  silence  of  pneumotnorax.  If  these 
fundamental  differences  prove  inadequate,  the  condition  of  the 
lung  opposite  the  hyperresonant  side  and  the  presence  of  definite 
pneumothoracic  adventitious  sounds  may  furnish  conclusive  evidence. 

One  must  occasionally  distinguish  circumscribed  pneumothorax 
from  a  large  s  iperficial  pulmonary  cavity,  owing  to  the  resemblance 
between  the  percussion  tympany  and  the  metallic  rales  elicited  in 
the  two  affections.  A  pulmonary  excavation,  rather  than  pneumo- 
thorax, is  indicated  by  localization  of  the  physical  signs  at  or  near 
the  apex  of  the  lung,  by  the  presence  of  a  circumscribed  area  of 


2Q4  PHYSICAL    DIAGNOSIS 

intercostal  immobility  and  retraction  in  this  situation,  and  by  finding 
little  or  no  dislocation  of  the  cardiac  apex,  which,  if  abnormally  placed, 
is  drawn  toward — not  pushed  away  from — the  lesion.  Additional 
evidence  in  favor  of  a  cavity  includes  intense  vocal  fremitus,  distinct 
pectoriloquy,  and  loud  amphoric  or  cavernous  breath-sounds,  in 
contradistinction  to  the  enfeebled  respiratory  and  voice-sounds 
ordinarily  detected  in  pneumothorax.  Though  such  signs  are 
most  extraordinary,  a  large  pulmonary  cavity,  if  distended  with  air 
and  partly  filled  with  fluid,  may  yield  succussion,  metallic  tinkling, 
and  even  the  bell  tympany  of  the  coin  test. 

Subphrenic  pyopneumothorax,  a  gas-containing  abscess  cavity 
situated  between  the  diaphragm  and  the  liver,  counterfeits  true 
pneumothorax,  especially  one  circumscribed  at  the  base  of  the  chest. 
If  the  gaseous  distention  be  excessive,  the  diaphragm  is  pushed  up 
to  a  high  level  and  the  lung  compressed,  with  the  result  that  both 
physical  signs  and  symptoms  develop  which  intimately  resemble 
those  of  an  intrapleural  effusion  of  air.  In  this  differentiation  the 
fluoroscope  is  most  helpful,  since  it  reveals,  over  a  subphrenic  pyo- 
pneumothorax, an  abnormally  high  diaphragm  shadow  beneath  the 
dome  of  which  is  a  clear,  luminous  tract,  indicative  of  air,  and 
sharply  contrasting  with  a  horizontal  zone  of  darkness  corresponding 
to  the  underlying  purulent  collection.  It  is  also  of  service  to  remem- 
ber that  a  subphrenic  abscess  is  usually  a  sequel  of  gastric  or  intestinal 
perforation  (as  in  gastric  or  duodenal  ulcer),  in  consequence  of 
which  the  subphrenic  space,  more  commonly  on  the  left  side,  becomes 
infected  by  material  and  distended  by  gas  derived  from  the  gastro- 
intestinal tract. 

In  a  rare  emergency  it  is  necessary  to  differentiate  pneumothorax 
and  diaphragmatic  hernia,  for  in  this  grave  accident  the  stomach 
and  gut,  ballooned  with  air,  may  protrude  through  a  rent  in  the 
diaphragm  into  the  thoracic  cavity,  thereby  faithfully  reproducing 
the  physical  conditions  and  signs  of  air  within  the  pleural  sac.  Evi- 
dence in  favor  of  hernia  includes  the  detection  of  gastro-intestinal 
rumbling  and  sibilant  noises  over  the  lower  thorax,  as  well  as  the 
important  fact  that  should  the  hernial  protrusion  suddenly  recede, 
as  it  sometimes  does,  both  signs  and  symptoms  will  disappear  coin- 
cidentally.  A  history  of  injury  is  no  sure  criterion,  since  it  may  be 
the  factor  of  either  condition.  Congenital  hernia  of  the  diaphragm 
is  occasionally  encountered. 

A  greatly  dilated  stomach,  in  so  far  as  it  can  account  for  tympany, 
succussion  sounds,  tinkling  noises,  and  embarrassed  respiration, 
must  be  reckoned  with  as  a  possible  mimic  of  left-sided  pneumothorax. 


DISEASES    OF   THE    BRONCHOPULMONARY   SYSTEM        295 

But  the  previous  history  of  the  two  conditions  is  radically  unlike,  and 
in  gastric  dilatation  there  is  no  distinctive  combination  of  signs, 
such  as  unilateral  distention  of  the  thorax,  descent  of  the  diaphragm, 
compression  of  the  lung,  and  conspicuous  displacement  of  the  heart. 

PLEURAL  NEOPLASMS 

Carcinoma. — The  great  majority  of  pleural  neoplasms  are 
secondary  to  carcinoma  of  the  lung,  which  invades  the  pleural  mem- 
branes by  direct  extension;  less  commonly  the  cancer  arises  by 
metastasis  from  a  primary  lesion  of  the  lung,  breast,  gullet,  or  thyroid. 
Unilateral  implication  is  the  rule,  affecting  the  right  pleura  somewhat 
more  commonly  than  the  left.  Ordinarily,  the  cancerous  lesions  con- 
sist of  multiple  nodules,  first  appearing  along  the  course  of  the  lym- 
phatics and  sometimes  becoming  so  large  as  to  excite  active  symptoms 
of  intrathoracic  pressure,  to  dislocate  the  mediastinum  and  its  con- 
tents, and  to  bulge  the  chest-wall.  Less  commonly  a  diffusely  dis- 
seminated type  of  growth  is  met  with,  the  pleural  membranes  being 
densely  infiltrated,  welded  together,  and  contracted,  with  the  result 
that  striking  deformity  of  the  chest  ensues  in  the  course  of  time. 
Cancer,  as  well  as  all  other  forms  of  pleural  neoplasm,  tends  ulti- 
mately to  excite  inflammation  of  the  pleura,  generally  with  an  effu- 
sion which  in  fully  two- thirds  of  all  cases  is  hemorrhagic. 

The  physical  signs  of  secondary  cancer  of  the  pleura  are  referable 
chiefly  to  the  primary  pulmonary  lesion  (see  p.  260),  and  secondarily 
to  the  presence  of  either  a  plastic  or  an  exudative  pleurisy.  If  the 
latter  exists,  as  is  usually  the  case,  an  exploratory  puncture  should 
be  made,  with  a  view  to  finding  in  the  aspirated  fluid  erythrocytes, 
free  fat,  cancerous  elements,  and  a  considerable  number  of  mitotic 
cells.  As  a  rule,  the  fluid  also  contains  relatively  few  lymphocytes 
and  many  large  vacuolated  endothelial  cells,  commonly  occurring  in 
plaques.  (See  p.  54.) 

Aside  from  the  important  signs  relating  to  the  primary  growth  in 
the  lung  or  some  other  locality,  severe  and  stubborn  pleural  pain, 
cervical  and  axillary  glandular  enlargements,  local  chest  deformity, 
and  a  cachectic  appearance  of  the  patient  are  to  be  regarded  as 
important  details  of  the  clinical  picture.  The  heart  may  be  displaced 
either  by  effusion  or  by  the  growth,  and  dense  adhesions  may  make 
the  displacement  permanent. 

Of  primary  carcinoma  of  the  pleura,  little  need  be  said,  for  the 
disease  is  more  often  discovered  by  the  pathologist  than  by  the 
clinician.  So  long  as  the  pleura  alone  is  implicated  the  physical 


296  PHYSICAL   DIAGNOSIS 

signs  suggest  merely  a  pleurisy,  dry  or  effusive,  for  the  constitutional 
evidences  of  malignant  disease  are  not  clearly  defined.  The  develop- 
ment of  metastases  (i.  e.,  in  the  lung,  liver,  or  superficial  lymphatics) 
is  of  distinct  diagnostic  aid,  if  such  findings  be  reviewed  in  the  light 
of  the  pleural  manifestations. 

Sarcoma. — Sarcoma  of  the  pleura  is  an  exceedingly  rare  affection, 
and  one  impracticable  to  distinguish  clinically  from  carcinoma, 
like  which  it  is  usually  accompanied  by  hemorrhagic  effusion,  severe 
pain,  deformity  of  the  chest,  and  moderate,  if  any,  cachexia. 
Invasion  of  neighboring  and  remote  structures  has  been  observed  in 
the  primary  form,  of  which  only  about  a  dozen  cases  have  been 
recorded.  Secondary  pleural  sarcoma  is  also  rarely  met  with,  but 
the  pleura  appears  to  be  more  susceptible  to  sarcomatous  than  to 
cancerous  implication  by  metastasis,  in  malignant  disease  primarily 
developing  in  other  regions  of  the  body. 

MEDIASTINITIS 

Simple  acute  mediastinitis  is  a  rare  affection,  and  its  recogni- 
tion during  life  can  only  be  hazarded.  If  the  inflammation  does 
not  subside  by  resolution,  its  usual  termination,  either  a  fibrous  over- 
growth or  suppuration  of  the  mediastinal  tissues,  may  supervene, 
the  clinical  picture  in  each  event  being  fairly  definite.  Though 
many  cases  must,  unfortunately,  be  dubbed  "idiopathic,"  in  others 
a  satisfactory  cause  is  at  hand,  such  as  trauma  and  inflammation 
of  the  pericardium  or  of  the  mediastinal  pleura;;  abrupt  suppression 
of  the  menses  is  a  doubtful  factor. 

Reliable  physical  signs  are  wanting  in  simple  acute  mediastinitis, 
the  existence  of  which  is  suggested  by  the  patient's  history  plus 
symptoms  such  as  severe  substernal  and  interscapular  pain,  per- 
sistent Irritative  cough,  and  moderate  fever  with  rigors. 

Chronic  mediastinitis  accounts  for  more  constant  and  active 
clinical  findings  than  the  acute  form,  since  it  consists  not  only  of  a 
mediastinal  fibrosis,  but  also  of  more  or  less  extensive  pericardial 
inflammation  and  adhesion.  Syphilis  is  a  prominent  factor  in  such 
cases,  and  intensive  treatment  with  salvarsan  is  most  helpful,  even 
in  the  face  of  definite  pressure  symptoms. 

Following  the  classification  of  Thomas  Harris,  three  patho- 
logic varieties  are  recognized:  those  in  which  there  are  both  ex- 
ternal and  internal  adhesions  of  the  pericardium,  great  increase 
of  mediastinal  fibrous  tissue,  and  often  caseation  of  the  medias- 
tinal lymphatic  glands  (the  indurative  mediastinopericarditis  of 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        297 

Kussmaul);  those  in  which  there  are  extensive  external  and  internal 
adhesions  of  the  pericardium,  but  little  or  no  mediastinal  fibrosis 
(the  so-called  external  and  internal  pericarditis) ;  and  those  in  which 
there  is  decided  mediastinal  fibrosis  attended  by  merely  external 
pericardia!  adhesion  (the  true  chronic  mediastinitis) . 

Mediastinopericarditis  is  attended  by  great  cardiac  hypertrophy 
and  dilatation,  by  chronic  hepatic  and  renal  congestion,  and  in 
some  instances  by  proliferative  peritonitis,  perisplenitis,  and  a  type 
of  perihepatitis  termed  pericarditic  pseudocirrhosis  or  Pick's  dis- 
ease. Bronchitis,  pleurisy,  and  pulmonary  fibrosis  are  familiar 
associated  conditions,  and  ascites,  with  or  without  general  dropsy, 
is  prone  to  occur,  especially  as  the  result  of  cardiohepatic  lesions, 
peritonitis,  and  venous  obstruction  due  to  mediastinal  pressure. 

The  physical  signs  of  chronic  mediastinitis  are  referable  mainly 
to  the  associated  lesions  of  the  heart  and  pericardium  and  to  the 
sequelae  arising  therefrom.  On  inspection,  there  is  seen  a  variable 
degree  of  thoracic  immobility  and  dyspnea,  perhaps  with  cyanosis, 
dropsy,  and  engorgement  of  the  cervical  and  thoracic  veins.  Inspira- 
tory  distention  of  the  right  external  jugular  vein  is  a  suggestive  though 
an  inconstant  sign:  it  indicates  obstruction  of  the  jugular  return 
flow,  due  to  compression  of,  or  traction  upon,  the  intrathoracic  veins, 
and  has  been  observed  also  in  simple  pericarditis,  in  pleurisy,  and 
in  mediastinal  tumor.  Palpation  over  the  sternum,  if  roughly  per- 
formed, may  provoke  lancinating  pain.  Of  frequent  occurrence 
is  the  paradoxic  pulse,  which  weakens  or  completely  disappears 
during  inspiration,  but  this  peculiarity  is  by  no  means  distinctive 
of  mediastinal  fibrosis.  (See  p.  338.)  Percussion  shows,  if  the 
fibrosis  be  extensive,  an  abnormal  area  of  dulness  over  and  aloi  igside 
the  sternum,  though  such  a  finding  is  more  often  the  result  of  the  car- 
diac enlargement  or  of  the  mediastinal  adenitis.  On  auscultation 
over  the  sternum  one  sometimes  hears  dry  crackling  mediastinal 
sounds  and  also  the  Eustace  Smith  hum  (v.  «'.),  while  the  rales  of 
bronchitis  and  the  friction-sounds  of  pericarditis  and  pleurisy  gener- 
ally coexist.  Evidences  of  cardiac  dilatation  and  hypertrophy,  of 
chronic  adhesive  pericarditis,  and  of  hepatic  (rarely,  splenic)  en- 
largement are  also  prominent  details  of  the  symptom-complex  in 
many  instances  of  chronic  mediastinitis. 

Suppurative  mediastinitis,  due  to  the  invasion  of  pyogenic  cocci, 
occurs  in  consequence  of  trauma  and  of  ulcerative  diseases  of  the 
air-passages  and  gullet;  it  results  also  from  the  extension  of  septic 
lesions  of  the  cervical  fascia,  the  tracheobronchial  glands,  the  lungs, 
and  the  pleurae;  and  it  may  be  secondary  to  actinomycosis  or  to  various 


298  PHYSICAL   DIAGNOSIS 

acute  infectious  diseases,  notably  erysipelas,  enteric  fever,  variola, 
and  pyemia.  The  suppuration  thus  set  up  may  occur  as  a  wide- 
spread purulent  infiltration  of  the  mediastinal  tissues,  or  as  one  or 
more  circumscribed  abscesses.  The  former  tends  to  run  an  acute 
and  rapidly  fatal  course,  attended  by  well-marked  evidences  of 
sepsis.  The  latter,  if  effectually  walled  in  by  a  pyogenic  membrane, 
often  remains  latent  for  a  long  period,  and  may  even  become  absorbed 
or  encapsulated;  or  the  abscess  may  burrow  through  the  mediastinal 
space  and  finally  discharge  through  the  line  of  least  resistance — into 
the  trachea,  a  bronchus,  or  the  esophagus,  through  an  intercostal 
space  or  downward  along  the  spine,  through  the  abdominal  wall, 
or  into  one  of  the  large  blood-vessels.  Tuberculous  abscesses  of 
the  mediastinum  are  usually  of  limited  extent,  and  do  not  give  rise 
to  severe  systemic  disturbances,  save  when  secondary  contamination 
with  pyogenic  microorganisms  takes  place.  Cold  abscess  of  the 
mediastinum  can  generally  be  traced  to  tuberculosis  of  the  medias- 
tinal glands,  or  to  caries  of  the  spine  or  chondrosternal  structures. 
It  is  the  general  belief  that  it  most  frequently  affects  the  posterior 
space,  while  the  other  spaces  suffer  chiefly  from  the  acute  form  (Hare) . 
The  physical  signs  of  mediastinal  suppuration  are  notoriously 
untrustworthy,  being  quite  negative  in  small  deep-seated  lesions. 
However,  in  a  large  abscess  of  the  anterior  or  superior  mediastinum 
inspection  not  infrequently  detects  a  dusky,  hot,  fluctuating  and 
sometimes  pulsating  swelling  in  the  sternal  region,  while  exceptionally 
actual  pointing  of  the  pus  through  the  chest-wall  is  observed.  The 
cardiac  apex  is  enfeebled  and  dislocated  in  relation  to  the  size  and 
situation  of  the  purulent  collection.  On  palpation  tenderness  over 
the  sternum  is  elicited,  and  the  local  peculiarities  of  the  swelling  are 
appreciated;  in  some  instances  there  is  a  paradoxic  pulse.  Percus- 
sion may  demonstrate  undue  upward  and  lateral  extension  of  cardiac 
dulness,  and  also,  in  a  large  abscess  of  the  posterior  mediastinum, 
a  dull  area  between  the  scapulae  on  either  side  of  the  spine.  Evi- 
dences of  mediastinal  pressure  (for  a  description  of  which  see  Medias- 
tinal Tumors,  p.  301)  arise,  should  the  situation  and  the  character 
of  the  abscess  be  such  as  to  crowd  the  important  vessels,  nerves,  and 
other  organs  of  the  mediastinum.  Such  symptoms  are,  as  a  rule, 
not  so  conspicuous  in  abscess  as  in  mediastinal  neoplasm. 

MEDIASTINAL  LYMPHADENITIS 

Adenitis,    either   simple   or   suppurative,    frequently   affects   the 
mediastinal  lymphatic  glands,   of  which  there  are  three  principal 


DISEASES    OF   THE    BRONCHOPULMONARY    SYSTEM        299 

groups :  those  lying  in  the  loose  areolar  tissue  of  the  anterior  space 
and  also  around  the  innominate  veins,  the  aortic  arch,  and  in  front 
of  the  trachea;  those  situated  along  the  esophagus  and  the  aorta  in 
the  posterior  space;  and  the  bronchial  group  of  the  middle  medias- 
tinum. Of  these,  the  last  named  is  of  peculiar  interest,  owing  to  its 
intimate  relation  with  the  bronchi  and,  through  afferents,  with  the 
lungs  and  pleurae. 

Simple  lymphadenitis,  with  engorgement  and  edematous  swelling 
of  the  glands,  attends  practically  all  bronchopulmonary  inflamma- 
tions— bronchitis,  bronchopneumonia,  influenza — and  occurs  with 
especial  frequency  in  the  bronchitides  of  measles  and  pertussis.  In 
the  latter  disease,  indeed,  the  paroxysmal  attacks  of  cough  and 
dyspnea  are  interpreted  by  de  Mussy  as  evidence  of  pressure  by  the 
enlarged  lymph-nodes  of  the  posterior  mediastinum.  Bronchial 
adenitis  is  an  almost  constant  autopsy  finding  in  pulmonary  tuber- 
culosis. 

Suppurative  lymphadenitis  is  generally  of  tuberculous  origin, 
but  it  occasionally  arises  as  the  sequel  of  simple  adenitis  due 
to  another  factor.  In  some  instances  the  suppuration  is  confined 
to  the  gland  or  group  of  glands  primarily  affected,  and  ultimately 
absorption  of  the  pus  and  calcification  of  the  lesion  may  take  place; 
in  other  cases  the  pus  burrows  and  finds  an  outlet,  as  by  fistulation 
into  a  bronchus  or  into  the  esophagus;  and  in  still  others  the  infec- 
tion may  extend  to  the  lungs  and  pleurae,  or  mediastinal  abscess  may 
develop.  In  tuberculous  adenitis  the  mediastinal  focus  of  infection 
may  account  for  the  supervention  of  an  acute  miliary  process 
and  for  phthisis,  the  former  being  due  to  the  perforation  of  a 
vessel  and  the  latter  either  to  direct  extension  of  the  lesion  or 
to  the  inspiration  of  tuberculous  material  which  has  eroded  a 
channel  into  a  bronchial  tube.  But  pulmonary  tuberculosis  and 
glandular  infection  are  by  no  means  constant,  even  in  long-standing 
tuberculous  caseation  of  the  lung — an  example,  Rist  suggests,  of 
allergy,  like  the  acquired  immunity  of  the  buccal  mucosa  in  phthis- 
ical subjects. 

The  physical  signs  of  mediastinal  lymphadenitis  are  rarely  definite 
enough  to  be  of  much  value,  save  in  an  occasional  case  of  extensive 
enlargement  of  the  anterior  mediastinal  glands,  in  which  abolished 
tactile  fremitus,  respiratory  silence,  and  dulness  are  detected  over 
and  alongside  the  sternum;  or  the  glandular  masses  may  exagge- 
rate the  bronchial  sounds,  combining  bronchophony  and  intensified 
breath  sounds  with  sternal  dulness.  In  some  instances  the  thoracic 
segment  of  the  spine  furnishes  a  group  of  most  suggestive  signs: 


300  PHYSICAL   DIAGNOSIS 

tenderness  from  the  second  to  the  seventh  spinous  tip;  dulness  over 
the  fifth  (normally  resonant);  and  a  patch  of  bronchial  breathing 
and  bronchophony  at  the  level  of  the  first.  The  writer  is  accus- 
tomed to  place  the  same  significance  on  the  combination  of  hypo- 
resonance  with  maximum  tactile  resistance  as  on  the  association 


Fig.  117. — Radiograph  of  mediastinal  lymphadenitis.     (Plate  by  Dr.  W.  F.  Manges.) 

of  hyperresonance  with  minimum  tactile  resistance  in  uncompli- 
cated adenopathies.  It  is  assumed,  to  explain  this  apparent  para- 
dox, that  in  the  former  instance  the  glandular  mass  exerts  a  dulling 
pressure,  and  that  in  the  latter  it  conducts  the  predominant 
tracheal  vibrations  to  the  vertebral  tips. 
It  is  frequently  possible  to  demonstrate  d'Espine's  sign  of 


DISEASES    OF    THE    BRONCHOPULMONARY    SYSTEM        30! 

tympany  combined  with  exquisitely  clear  whispering  pectoril- 
oquy  over  the  upper  thoracic  vertebral  spinous  processes,  and 
this  sign  is  dependable  as  an  early  and  most  constant  clue  to 
adenopathies  which,  by  structure  and  situation,  act  as  effectual 
transmission  paths  for  sounds  generated  within  the  large  air- 
passages. 

Tracheobronchial  tumors  may  compress  the  left  innominate  vein 
when  the  subject's  head  is  stretched  far  backward,  and  thus  pro- 
duce a  venous  hum  audible  over  the  manubrium — Eustace  Smith's 
murmur.  Paroxysmal  cough,  dyspnea,  hoarseness,  and  dilatation 
of  the  venules  upon  the  anterior  surface  of  the  thorax  are  pressure 
symptoms  of  decided  importance.  In  children  persistent  dry 
cough,  with  negative  surface  signs,  may  be  referable  to  enlargement 
of  the  lymph-nodes  at  the  tracheal  bifurcation,  especially  those 
situated  below  the  right  bronchus.  Herbert  French  attributes  the 
cough  in  such  cases  to  irritation  of  the  phrenic  nerve. 

An  #-ray  examination  usually  reveals  the  presence  of  enlarged 
mediastinal  glands,  even  at  an  early  stage  of  their  development 
(Fig.  117).  The  shadow  cast  by  a  group  of  hypertrophied  bronchial 
glands  suggests  aortic  aneurism,  but  an  aneurismal  shadow  may 
show  pulsation,  and  on  inspection  from  various  directions  can 
generally  be  localized  to  some  part  of  the  aortic  arch.  In  adult 
life  the  normal  pulmonary  radiograph  ordinarily  shows  small  isolated 
glandular  shadows,  for  few  persons  reach  maturity  without  at  some 
time  having  been  subject  to  a  bronchopulmonary  irritation  whereby 
permanent  adenoid  enlargement  is  excited.  In  Fig.  70,  a  radio- 
graph of  a  perfectly  normal  thorax,  the  shadows  alongside  the 
mediastinal  area  indicate  this  wholly  benign  type  of  glandular 
enlargement,  which  is  without  pathologic  significance. 

MEDIASTINAL  NEOPLASMS 

C'inical  Pathology. — Sarcoma  and  carcinoma  are  the  most 
important  types  of  malignant  tumors  affecting  the  mediastinal 
spaces,  the  former  being  decidedly  the  commoner  of  the  two  and 
more  likely  to  be  of  primary  origin.  Primary  sarcoma  may  arise 
from  the  thymus  gland  or  its  remains,  or  from  the  lymphatic  glands, 
the  pleuropulmonary  structures,  and  the  mediastinal  tissues;  second- 
ary tumors  of  this  type  are  generally  the  sequel  of  an  initial  growth 
in  some  distant  part.  Primary  carcinoma  more  commonly  springs 
from  the  esophagus  or  the  bronchopulmonary  structures  than  from  the 
thymus  or  connective  tissue;  secondary  cancer  of  the  mediastinum 


302  PHYSICAL   DIAGNOSIS 

is  prone  to  develop  in  the  neighborhood  of  the  primary  tumor. 
Among  the  rarer  solid  tumors  of  the  mediastinum  are  included 
the  simple  lymphomata,  and  also  growths  of  gummatous,  fibrous, 
cartilaginous,  osseous,  and  teratomatous  character.  Of  cystic 
tumors,  hydatids  and  dermoids  are  examples  exceptionally  ob- 
served. The  anterior  mediastinum  is  the  most  common  situation 
of  malignant  disease,  and  here  is  the  selective  site  of  sarcomatous 
lesions;  for  the  posterior  space  carcinoma  apparently  has  a  pre- 
dilection. Not  only  does  the  mediastinal  tissue  become  the  seat  of 
extensive  malignancy,  but  its  important  organs  as  well  as  the  neigh- 
boring structures  also  share  in  the  change.  Compression  of  the 
mediastinal  vascular  trunks,  nerves,  air-passages,  and  esophagus 
is  produced,  the  pleurae,  lungs,  pericardium,  and  even  the  heart 
may  become  implicated,  and  in  some  instances  the  growth  encroaches 
upon  the  neck,  extends  through  the  diaphragm,  or  presses  against 
the  anterior  or  the  posterior  chest-wall.  Metastatic  spread  of  the 
original  growth  is  also  likely  to  take  place  via  the  blood  or  the 
lymphatic  vessels. 

For  clinical  study  it  is  convenient  to  divide  mediastinal  tumors 
into  two  main  groups:  those  of  the  anterior  and  superior  mediastinal 
spaces,  in  which  the  physical  signs  overshadow  the  pressure  phe- 
nomena; and  those  situated  in  the  middle  and  posterior  mediastina, 
in  which  the  physical  signs  are  subordinate  to  the  pressure  symptoms. 
It  is  perfectly  obvious  that  this  purely  arbitrary  classification  is  of 
limited  applicability,  since  neoplasms  tend  progressively  and  erratic- 
ally to  invade  the  different  mediastinal  compartments,  thus  giving 
rise  to  a  medley  of  symptoms  relating  partly  to  this  and  partly  to 
that  space.  Despite  this,  in  order  to  trace  the  origin  of  such  symp- 
toms, it  is  well  to  have  a  mental  picture  of  these  chief  mediastinal 
compartments  and  of  the  effects  produced  upon  their  contents  by  the 
encroachment  of  morbid  new-growths. 

Physical  Signs. — Tumors  of  the  Anterior  and  Superior  Medias- 
tinum.— The  principal  signs  of  growths  situated  immediately  beneath 
the  sternum  relate  to  the  contour  of  the  anterior  chest-wall,  to  the 
consequences  of  compression  or  occlusion  of  the  superior  vena  cava 
and  the  innominate  veins,  and  to  irritation  of  the  superior  laryngeal 
and  sympathetic  nerves. 

Inspection. — It  is  of  some  interest  to  note  that  the  subject  of  a 
malignant  tumor  in  this  situation  is  anemic  rather  than  character- 
istically cachectic,  and  that  emaciation,  though  it  does  occur,  is  not 
usually  conspicuous  until  the  disease  has  almost  run  its  course. 
Clubbing  of  the  finger-tips  generally  develops  in  cases  of  long  standing. 


DISEASES   OF   THE   BRONCHOPULMONARY   SYSTEM          303 

Dyspnea  is  usually  moderate,  so  long  as  the  growth  does  not 
encroach  far  in  a  backward  direction.  As  the  result  of  persistent 
intrathoracic  pressure  the  sternum  finally  gives  way,  and  bulges  out- 
ward to  form  a  mound-like  swelling  (Fig.  118),  or  the  growth  may 
erode  the  chest-wall,  appearing  thereupon  as  a  circumscribed  node, 
of  variable  size,  outline,  and  consistence,  but  tending  ultimately 
to  soften,  to  discolor,  and  to  break  down.  Occlusion  of  the  intra- 


Fig.  1 1 8. — Bulging  of  the  thorax  in  a  case  of  mediastinal  neoplasm  (Jefferson 

Hospital). 

thoracic  venous  trunks  accounts  for  edema  and  for  distention  and 
tortuosity  of  the  superficial  veins  of  the  face,  neck,  arms,  and  upper 
anterior  chest- wall,  bilateral  phenomena  of  this  sort  indicating 
superior  caval  obstruction,  and  unilateral  signs  pointing  to  com- 
pression of  an  innominate  vein  or  one  of  its  tributaries.  The  illus- 
tration elsewhere  shown  (Fig.  51,  p.  106)  gives  a  good  idea  of  the 
appearance  of  engorged  superficial  veins  upon  the  surface  of  the 


304  PHYSICAL   DIAGNOSIS 

body.  Inequality  of  the  pupils  is  not  a  frequent  sign  in  growths  af- 
fecting the  anterior  mediastinum,  owing  to  the  posterior  position 
of  the  sympathetic  nerve.  Hoarseness  and  loss  of  voice,  from  com- 
pression of  the  inferior  laryngeal,  are,  however,  very  common  find- 
ings. 

Palpation. — Pressure  over  the  sternum  is  painful  to  the  patient, 
and  palpation  may  detect  a  systolic  pulsation  over  the  tumor,  the 
density  of  which  ranges  from  stony  hardness  to  soft  edema.  The 
lifting  throb  of  a  soft,  overvascular  tumor  must  be  carefully  dis- 
tinguished from  the  expansile  pulsation  of  an  aneurism.  Tactile 
fremitus  is  usually  abolished  over  the  growth  and  its  infiltrative 
extensions.  In  some  instances  the  primary  growth  is  palpable  in 
the  suprasternal  notch,  and  secondary  glandular  enlargements  appear 
in  the  neck  and  in  the  axillae. 

Percussion. — There  is  an  area  of  dulness  or  of  flatness  correspond- 
ing to  the  site  of  the  tumor,  in  the  immediate  neighborhood  of  which 
hyperresonance  is  the  rule.  Abnormal  modifications  of  the  per- 
cussion sound  are  also  likely  to  be  found  over  other  parts  of  the  thorax, 
where  associated  pulmonary  and  pleural  lesions  exist. 

Auscultation. — Ordinarily,  the  respiratory  murmur  is  suppressed 
over  the  tumor  and  exaggerated  over  the  adjacent  lung,  but  some- 
times the  growth  distinctly  conducts,  or  even  intensifies,  the  breath- 
sounds.  Bronchial  rales,  pleural  and  pericardial  friction-sounds, 
and  systolic  murmurs  due  to  compression  of  the  aorta  and  pulmonary 
artery  are  audible  in  certain  cases.  The  cardiac  sounds  are  fre- 
quently, though  not  invariably,  obscure,  muffled,  and  distant,  par- 
ticularly at  the  base. 

Tumors  of  the  Middle  and  Posterior  Mediastinum. — In  this  situation 
growths,  even  of  moderate  size,  cause  signs  referable  mainly  to  com- 
pression of  the  vagus,  the  bronchi,  and  the  gullet,  while  in  some 
instances  there  are  evidences  of  pressure  upon  the  azygos  veins  and 
the  inferior  vena  cava,  as  well  as  of  extensive  necrosis  of  the  parts 
encroached  upon. 

Inspection. — True  cachexia,  emaciation,  asthenia,  and  fever  are 
more  common  than  in  lesions  of  the  anterior  mediastinal  space. 
The  patient  is  constantly  dyspneic  and  subject  to  alarming  paroxysms 
of  orthopnea,  stridulous  breathing,  brassy  cough,  and  dysphagia, 
due  chiefly  to  vagus  irritation,  but  in  part  to  compression  of  the 
bronchopulmonary  structures.  Syncope,  vomiting,  symmetric  cold- 
ness of  the  extremities,  and  disturbances  of  the  cardiac  rate,  rhythm, 
and  force  also  occur  as  the  result  of  what  Cowers  terms  "vagal 
attacks."  The  pulse,  aside  from  its  irregularity,  is  of  feeble  volume 


DISEASES   OF   THE   BRONCHOPULMONARY  SYSTEM         305 

bilaterally,  if  the  aorta  be  compressed,  while  differences  in  the 
force  of  the  two  radials  is  noticed  in  the  event  of  pressure  upon 
the  innominate  artery  or  upon  the  left  subclavian.  Edema  of  the 
lower  extremities,  ascites,  and  engorgement  of  the  surface  tribu- 
taries of  the  inferior  vena  cava  are  visual  evidences  of  constriction 
of  this  great  venous  trunk.  Inequality  of  the  pupils,  and  some- 


Fig.  119. — Radiograph  of  a  mediastinal  neoplasm.  Lateral  aspect,  showing 
dense  shadow  in  the  anterior  mediastinum,  with  infiltration  of  the  sternum,  and 
edema  of  the  overlying  chest-wall.  (Plate  by  Dr.  W.  F.  Manges.) 

times  unilateral  circumscribed  flushing  and  perspiration,  betoken 
irritation  of  the  sympathetic  cord. 

Palpation. — Considerable  significance  attaches  to  the  sign  noted 
by  Graham  Steel  1,  who  observed  that  the  visible  and  palpable  cardiac 
impulse  covers  an  area  almost  coextensive  with  that  of  the  entire 
heart,  which,  when  encroached  upon  by  a  tumor  of  the  posterior 


306 


PHYSICAL   DIAGNOSIS 


mediastinum,  appears  to  thrust  itself  forward  en  masse  with  every 
systole.  In  other  cases,  where  this  diffuse  impulse  is  not  present, 
the  apex-beat  may  merely  be  tilted  outward  and  downward  away 
from  its  normal  site. 

Percussion. — Ordinarily,  a  tumor  deep  within  the  mediastinum  is 
far  beyond  the  reach  of  percussion,  although  should  it  extend  back- 
ward against  the  posterior  wall  of  the  thorax,  a  patch  of  irregularly 
shaped  dulness  or  flatness  may  be  delimited  in  the  interscapular 
region.  It  is  not  uncommon  to  find  the  basal  flatness  of  intrapleural 
fluid,  poured  out  usually  as  the  result  of  an  associated  pleurisy,  and 
exceptionally  by  fault  of  pressure  stasis  within  an  azygos  vein.  The 
percussion  findings  of  pulmonary  edema,  excited  by  pressure  upon 


Fig.  120. — Radiograph  of  a  mediastinal  neoplasm.  Anterior  aspect,  showing 
abnormal  extension  and  density  of  the  mediastinal  shadow,  with  displacement  of  the 
heart.  (Plate  by  Dr.  W.  F.  Manges.) 

the  pulmonary  veins,  and  of  a  distended  right  heart,  due  to  pul- 
monary artery  compression,  are  present  in  certain  cases. 

Auscultation. — Of  especial  interest  in  connection  with  neoplasm  of 
the  middle  and  posterior  mediastina  are  the  physical  signs  of  bronchial 
occlusion,  partial  or  complete.  (See  p.  184.)  Aside  from  this, 
evidences  of  recurrent  laryngeal  nerve  implication  and  of  secondary 


DISEASES    OF   THE    BRONCHOPULMONARY   SYSTEM         307 

lesions  of  the  lungs,  pleurae,  and  pericardium  should  be  given  due 
attention. 

Diagnosis. — Usually  it  is  not  difficult  to  recognize  mediastinal 
pressure,  but  it  is  quite  another  matter  to  prove  that  the  pressure 
is  due  to  malignant  disease  unless  the  case  presents  classic  symptoms 
and  signs.  The  association  of  persistent  dyspnea,  dysphagia,  sub- 
sternal  and  interscapular  pain,  venous  obstruction,  and  nervous 
symptoms  constitutes  a  syndrome  scarcely  to  be  misinterpreted, 
especially  in  the  face  of  the  physical  signs  of  an  intrathoracic  tumor 
in  a  person  who  has  steadily  lost  weight,  failed  in  strength,  and 
become  anemic  or  cachectic.  These  signs  having  been  obtained,  in 
part  or  as  a  whole,  it  is  perhaps  justifiable  to  predict  sarcoma  when 
the  lesion  affects  the  anterior  mediastinum,  grows  rapidly,  attains 
a  large  size,  and  provokes  striking  local  signs;  and  it  seems  also 
warranted  to  diagnose  carcinoma  when  the  growth  occupies  the  pos- 
terior mediastinum,  develops  slowly,  and  is  accompanied  by  few, 
if  any,  local  manifestations.  The  radiograph  is  an  invaluable  aid 
in  both  the  direct  and  the  differential  diagnosis,  provided  that  its 
interpretation  be  sane  and  conservative.  (See  Figs.  119  and  120.) 

Aneurism  of  the  aortic  arch  is  the  lesion  most  often  confused  with 
mediastinal  tumor,  and,  indeed,  it  is  sometimes  quite  impossible  to 
make  the  antemortem  differentiation.  Diastolic  shock,  tracheal 
tugging,  cardiac  hypertrophy,  true  expansile  pulsation,  and  an 
absence  of  glandular  enlargement  are  in  favor  of  aneurism,  and  a 
history  of  syphilis,  unduly  severe  pain,  and  temporary  amelioration 
of  the  symptoms  after  the  use  of  the  iodids  make  this  inference  the 
stronger.  Furthermore,  an  aneurismal  swelling  generally  occupies 
a  higher  level  upon  the  anterior  chest-wall  than  a  growth  pushing 
forward  from  the  mediastinum,  and  the  development  of  the  former 
is  slower  and  the  patient's  lease  on  life  longer,  as  a  rule,  than  in 
malignant  tumor.  The  fluoroscope  reveals,  in  aneurism,  a  shadow 
that  may  clearly  show  expansile  pulsation  situated  along  the  course 
of  the  aorta,  while  the  shadow  cast  by  a  solid  growth  appears  as  an 
irregularly  shaped  extension  of  the  mediastinal  darkness  which  may 
or  may  not  throb  with  cardiac  systole. 

The  differentiation  of  malignant  disease  versus  gumma  of  the 
mediastinum  has  been  referred  to  elsewhere.  (See  p.  240.) 


SECTION   V 


EXAMINATION  OF  THE  CARDIOVASCULAR 
SYSTEM 


CLINICAL  ANATOMY 

THE  heart  and  its  pericardia!  investment  occupy  the  middle  medi- 
astinal  space  behind  the  lower  two-thirds  of  the  sternum,  the  long 
axis  of  the  organ  being  almost  horizontal,  and  its  greater  part 
projecting  to  the  left  of  the  median  line  of  the  trunk.  The  normal 
mm^im^^^,^  adult's  heart  weighs  approxi- . 
mately  from  9  to  n  ounces 
(255  to  310  gm.),  and  shows 
maximum  measurements  of 
about  5  inches  (12.5  cm.)  in 
length,  3^  inches  (8.75  cm.) 
in  width,  and  2\  inches  (6.25 
cm.)  in  thickness.  The  ca- 
pacity of  each  ventricle  is 
approximately.  3 \  ounces  (100 
c.c.),  according  to  Tigerstedt, 
and  the  auricles  are  capable 
of  holding  virtually  the  same 
volume  of  blood.  The  general . 
shape  of  the  heart  is  tha't  of 
a  blunt,  somewhat  flattened 
cone,  having  its  base  directed 
upward,  its  anterior  convex 
surface  placed  upward  and 
forward,  and  its  compara- 
tively flat  surface  facing  down- 
ward and  backward. 


Fig.  121. — Surface  topography  of  the  heart. 


The  pericardium  consists  of  an  outer  fibrous  and  an  inner  serous 
layer,  whereby  the  heart  is  completely  enveloped,  the  viscus  hanging 
free  therein  from  its  basal  attachment  to  the  great  vessels;  with  the 
308 


EXAMINATION   OF   THE    CARDIOVASCULAR    SYSTEM 


309 


fibrous  layers  of  the  latter  the  outer  pericardium  is  continuous,  while 
below  it  is  anchored  to  the  central  tendon  of  the  diaphragm.  The 
inner  pericardium  is  a  closed  sac  formed  by  two  serous  layers:  a 
parietal,  which  lines  the  fibrous  pericardium,  and  a  visceral,  which 
covers  the  heart  and  is  reflected  therefrom  along  the  great  vessels. 
Like  the  heart,  the  pericardium  is  of  a  roughly  conic  shape,  but  unlike 
the  cardiac  cone  whose  base  lies  upward,  the  pericardial  cone  has 
its  base  directed  downward.  

The  Precordia  (Fig.  122). 
— The  term  precordia,  or  pre- 
cordial  region,  designates  that 
area  of  the  anterior  chest-wall 
which  overlies  the  heart,  and 
corresponds  not  only  to  the 
part  of  the  organ  directly  im- 
pinging upon  the  inner  surface 
of  the  thorax,  but  also  to  the 
portion  overlapped  by  the 
pulmonary  margins.  The 
precordia,  therefore,  includes 
within  its  boundaries  both  the 
area  of  cardiac  flatness  and 
the  area  of  cardiac  dulness 
(q.  v.  i.~).  The  relations  of 
the  heart  to  the  chest-wall 
given  below  are  those  of  the 
average  normal  adult,  and 
more  or  less  regional  differ- 
ences must  be  expected  in  the 
individual  case,  owing  to  the  influence  of  age,  the  state  of  the  thoracic 
musculature  and  bony  structures,  and  the  development  of  the  lungs. 

The  base  of  the  heart,  consisting  of  the  two  auricles,  lies  in  front 
of  the  descending  thoracic  aorta  and  the  lower  right  pulmonary 
vein,  being  directed  upward,  backward,  and  to  the  right.  It  extends 
anteriorly  from  a  point  ^  inch  (1.25  cm.)  to  the  right  of  the  sternum 
to  a  point  i  inch  (2.5  cm.)  to  the  left  of  this  bone,  at  the  level  of  the 
upper  border  of  the  third  rib;  posteriorly,  the  base  extends  from  the 
fifth  to  the  eighth  thoracic  vertebra,  inclusive.  The  right  auricle 
lies  beneath  and  somewhat  external  to  the  right  half  of  the  sternum, 
between  the  third  and  the  sixth  costal  cartilages,  but  the  greater 
part  of  the  left  auricle  lies  posteriorly,  its  appendage,  beneath  the 
second  left  intercostal  space,  being  the  only  portion  of  this  chamber 
to  project  toward  the  anterior  surface  of  the  thorax.  The  auriculo- 


Fig.  122. — The  precordial  and  supracardiar 
areas. 


310  PHYSICAL   DIAGNOSIS 

ventricttlar  groove,  separating  the  auricles  from  the  ventricles,  is 
indicated  by  a  line  extending  from  midsternum,  at  the  level  of  the 
lower  border  of  the  third  costal  cartilage,  to  the  sixth  right  chondro- 
sternal  junction. 

The  right  border  of  the  heart,  formed  by  the  right  auricle,  is 
represented  by  a  line  running  from  the  right  extremity  of  the  base 
(upper  border  of  the  third  rib,  £  inch  (1.25  cm.)  from  the  sternum) 
to  the  sixth  right  chondrosternal  articulation,  and  curving  outward 
between  these  two  points  to  attain  a  maximum  convexity  in  the  fourth 
intercostal  space,  which  is  crossed  i£  inches  (3.75  cm.)  from  the 
midsternal  line. 

The  left  border  of  the  heart,  corresponding  to  the  left  ventricle, 
follows  a  line  curving  slightly  outward  from  the  left  extremity  of  the 
base  (upper  border  of  the  third  rib,  i  inch  (2.5  cm.)  from  the  sternum) 
to  the  anatomic  cardiac  apex  (q.  v.  i.) ,  situated  in  the  fifth  left  inter- 
costal space,  in  the  midclavicular  line.  From  somewhat  to  the  right 
of  this  point  the  interventricular  groove,  dividing  the  ventricles,  runs 
anteriorly  upward  to  the  third  left  chondrosternal  junction. 

The  lower  border  of  the  heart,  formed  almost  entirely  by  the 
right  ventricle,  though  to  a  slight  extent  by  the  left  ventricle,  is  mapped 
out  by  drawing  a  line  from  the  apex  to  the  lower  extremity  of  the 
right  border  (sixth  right  chondrosternal  articulation),  which  line 
crosses  the  xiphoid  cartilage  just  below  its  sternal  attachment. 

The  cardiac  valves  and  orifices  are  included  within  the  boun- 
daries of  a  flattened  circle,  extending  obliquely  across  the  body  of 
the  sternum  from  the  third  left  to  the  sixth  right  chondrosternal 
articulation  (Fig.  134).  From  above  downward  the  valves  lie  in  the 
following  order:  pulmonic,  at  the  upper  border  of  the  third  left 
chondrosternal  joint;  aortic,  beneath  the  left  half  of  the  sternum,  at 
the  lower  border  of  the  third  costal  cartilage;  mitral,  beneath  the 
left  half  of  the  sternum,  at  the  level  of  the  fourth  costal  cartilage; 
and  tricuspid,  extending  from  midsternum,  at  the  level  of  the  fourth 
costal  cartilage,  to  the  fifth  right  chondrosternal  junction.  The 
foregoing  landmarks  refer  only  to  the  anatomic  sites  of  the  valves, 
the  individual  tones  of  which  and  the  murmurs  pertaining  thereto 
are  most  clearly  audible  over  that  area  of  the  thorax  where  the  valve's 
chamber  approaches  c'osest  to  the  surface.  These  sites,  known  as 
"  valve  areas,"  or  "auscultatory  areas."  are  referred  to  in  connection 
with  auscultation  of  the  heart.  (See  p.  356.) 

The  Supracardiac  Vascular  Area  (Fig.  122). — The  great  blood- 
vessels arising  from  the  bare  of  the  heart  lie  within  a  rectangular 
area  extending  from  the  clavicles  to  the  cardiac  base  line,  and  bounded 
on  either  side  by  vertical  lines  projected  upward  from  the  latter's 


EXAMINATION   OF    THE   CARDIOVASCULAR   SYSTEM         311 

right  and  left  extremities.  This  space,  then,  overlies  the  superior 
vena  cava,  the  aortic  arch,  the  innominate  artery,  and  the  innominate 
veins.  The  superior  vena,  cava  extends  from  the  confluence  of  the 
innominate  veins,  at  the  right  sternoclavicular  joint,  to  its  outlet 
into  the  right  auricle,  at  the  third  chondrosternal  articulation,  the 
course  of  the  vessel  between  these  two  points  lying  beneath  and 
somewhat  external  to  the  right  sternal  edge.  The  ascending  aorta 
lies  behind  the  sternum  between  the  third  left  chondrosternal  junction 
and  the  second  right  costal  (or  aortic)  cartilage.  At  this  point  the 
aortic  arch  commences,  and  runs  thence  obliquely  upward  and  back- 
ward toward  the  fourth  thoracic  vertebra,  where  it  becomes  con- 
tinuous with  the  descending  thoracic  aorta;  the  highest  point  of  the 
aortic  arch  in  the  median  line  usually  lies  i  inch  (2.5  cm.)  below  the 
suprasternal  notch,  or  at  about  the  center  of  the  manubrium.  The 
ptilmonary  artery  runs  along  the  left  sternal  border  beneath  the 
second  intercostal  space  and  the  second  costal  cartilage.  The 
innominate  artery,  arising  from  the  upper  aspect  of  the  aortic  arch, 
runs  obliquely  upward  to  the  right  sternoclavicular  junction,  where 
it  divides  into  the  right  subclavian  and  common  cartoid  arteries; 
on  the  left  side  these  two  vessels  spring  from  the  aortic  arch  between 
its  middle  and  posterior  extremity,  the  common  carotid  coursing 
obliquely,  and  the  subclavian  running  almost  vertically,  upward 
into  the  neck.  Of  the  two  innominate  veins,  the  right  lies  under 
the  inner  extremity  of  the  right  clavicle,  and  the  left,  beneath  the 
upper  portion  of  the  manubrium. 

MECHANISM  OF  THE  CIRCULATION 

The  Cardiac  Cycle. — This  term  refers  to  the  series  of  events  that 
attend  each  beat  of  the  heart,  whose  cycle,  therefore,  comprises  the 
systole  or  contraction  of  the  auricles,  the  systole  or  contraction  of  the 
ventricles,  and  the  period  of  diastole  or  relaxation  and  passivity 
of  both  auricles  and  ventricles.  In  a  clinical  sense,  the  words  systole 
and  diastole,  when  used  without  a  qualifying  adjective,  mean  con- 
traction and  relaxation,  respectively,  of  the  ventricles.  Normally, 
the  systolic  and  diastolic  phases  on  the  right  and  left  sides  of  the 
heart  are  precisely  synchronous,  the  auricles  contracting  and  relaxing 
at  exactly  the  same  moment,  and  the  ventricles  doing  likewise.  The 
entire  cardiac  cycle  lasts  0.8  second,  of  which  o.i  second  is  occupied 
by  the  auricular  systole,  0.3  second  by  the  ventricular  systole,  and 
0.4  second  by  the  diastole  of  all  four  chambers.  Acceleration  of  the 
cardiac  action,  which  abbreviates  each  of  these  cyclic  phases,  especially 
affects  the  diastolic.  The  component  parts  of  the  cardiac  cycle 


312 


PHYSICAL   DIAGNOSIS 


and  their  relation  to  the  cardiac  sounds  and  impulses  are  graphic- 
ally shown  by  the  accompanying  diagram  (Fig.  123). 

The  origin  and  maintenance  of  the  cardiac  cycle  are  best  explained 
by  assuming  an  inherent  automatic  rhythmicity  of  the  myocardium, 
whereby  orderly  waves  of  contraction  are  generated  at  the  venous 
end  of  the  heart  and  are  conducted  thence  throughout  the  organ 
by  its  musculature.  This  myogenic  theory  of  the  heart-beat  attrib- 
utes to  the  cardiac  muscular  fibers  the  functions  of  "rhythmicity, 
excitability,  contractility,  conductivity,  and  tonicity"  (Gaskill), 


"Radial      Pulse. 


Pause. 


^/Jur. 
•Systole. 


Venfneu/ar 


Passive  Period. 


tuncular    Diastole. 


Venfr/cu/ar    J)ias/bie. 


Fig.  123. — The  events  of  the  normal  cardiac  cycle. 

whereby  the  heart  can  beat  independently  of  nerve  control,  the  vagus 
and  the  sympathetic  nerves  merely  regulating  the  force  and  the  rate 
of  the  contractions.  These  are  probably  excited  directly  by  certain 
inner  stimuli  due  to  the  action  of  ionized  salts  (especially  sodium, 
calcium,  and  potassium  ions)  in  solution  in  the  juices  of  the  tissues. 

Opposed  to  the  foregoing,  the  neurogenic  theory  of  the  heart-beat 
takes  for  granted  that  inner  stimuli  exciting  cardiac  contractions  arise 
in  the  intrinsic  nerve-cells  of  the  auriculovenous  area,  whence  impulses 
travel,  via  nerve  paths,  to  subsidiary  nerve-centers,  through  which  the 
auricular  and  ventricular  "con  tractions  are  activated.  This  theory, 
which  is  unsupported  by  positive  proof,  burdens  the  intrinsic  cardiac 
nerves  with  the  spontaneity,  the  orderly  sequence,  and  the  harmonious 
relations  of  the  several  events  of  the  cardiac  cycle. 

The  Cardiac  Movements. — The  earliest  phase  of  the  cardiac 
cycle  is  a  quivering  contractile  movement  at  the  mouths  of  the  venae 
cavae  and  pulmonary  veins,  presumably  initiated  at  the  caval  orifice 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       313 

in  a  minute  node  of  primitive  tissue  representing  the  remains  of  the 
sinus  venosus — the  sino-auricular  node  of  Keith  and  Flack.  Sys- 
tole of  the  auricles  immediately  follows,  as  the  peristaltic  wave 
extends  downward  through  the  musculature  of  these  chambers, 
to  the  auriculoventricular  bundle  of  His,  which  arises  from  a  node 
in  the  wall  of  the  right  auricle  (Tawara's  auriculoventricular  node) 
and  is  distributed  through  the  ventricular  musculature.  After  a 
momentary  delay  as  it  crosses  the  auriculoventricular  bridge  of  mus- 
cle, the  contraction  traverses  the  ventricles,  first  downward  through 
the  wall  toward  the  apex,  and  finally  inward  to  terminate  in  the  pap- 
illary muscles.  , 

The  recent  work  of  Kent  suggests  that  cardiac  impulses  also  may 
arise  spontaneously  in  a  mass  of  nodal  tissue  situated  in  the  lateral 
aspect  of  the  right  auricle,  and  pass  thence  downward  into  the 
ventricles  along  a  muscular  channel  connecting  the  upper  and  the 
lower  chambers  of  the  heart.  In  the  event  of  the  destruction  of 
His'  bundle  it  is  possible  that  impulses  are  conducted  to  the 
ventricle  along  this  right  lateral  bridge  of  Kent. 

The  ventricular  systole  thus  excited  is  followed  by  auricular 
diastole,  which  begins  as  the  earliest  waves  of  contraction  pass 
through  the  ventricles.  The  latter,  after  having  ejected  their 
contents  into  the  arterial  system,  relax  in  diastole,  and  this  final 
phase  of  the  cycle  is  succeeded  by  a  relatively  long  resting  period 
which  ushers  in  the  next  series  of  contractions  at  the  auricular  out- 
lets of  the  great  veins.  During  its  contraction  the  heart  twists  for- 
ward upon  its  long  axis  from  left  to  right,  the  ventricles  harden, 
shorten,  and  thicken,  and  the  apex,  now  pointed,  tilts  upward  and  to 
the  right;  the  auricles  diminish  in  size  and  recede,  while  the  aorta 
and  pulmonary  artery  distend  and  lengthen.  With  diastole  the 
heart  rotates  backward  and  to  the  left,  the  ventricles  become 
flaccid  and  globular,  the  apex  becomes  rounded  and  shifts  down- 
ward and  to  the  left;  the  auricles  distend  and  protrude,  and  the 
aorta  and  pulmonary  artery  collapse  and  shorten.1 

With  auricular  systole  the  blood  in  the  auricles  is  forced  through 
the  auriculoventricular  orifices  into  the  relaxed  ventricles.  Reflux 
into  the  venae  cavae  and  pulmonary  veins  (which  are  not  guarded  by 
valves  at  their  outlets)  is  prevented  by  several  factors:  chiefly  by  the 

1  Williams  and  James  have  proved,  by  electrocardiographic  tracings,  that 
there  may  be  a  true  reversal  of  the  cardiac  action,  the  ventricles  contracting 
before  the  auricles  and  the  impulses  initiated  in  the  lower  chambers  passing  up 
His'  bundle  into  the  auricular  muscle.  Such  a  condition  is  referable  to  a 
prevailing  dominance  of  the  intrinsic  ventricular  rhythm  over  the  normal  sinus 
rhythm  whereby  the  feebler  stimuli  of  the  latter  are  overshadowed. 


314  PHYSICAL   DIAGNOSIS 

low  intra-auricular  pressure,1  but  partly  by  the  constriction  of  the 
venous  orifices  by  the  contraction  of  their  muscular  coats,  as  well  as 
by  the  free  outlet  afforded  the  blood-stream  by  the  widely  dilated 
mitral  and  tricuspid  openings. 

The  ventricular  diastole,  which  coincides  with  the  entire  systole  of 
the  auricles  and  with  the  last  part  of  their  diastole,  is  due  mainly  to 
the  inherent  resiliency  of  these  chambers.  During  this  period  the 
ventricles  fill  with  blood,  which  gradually  floats  up  the  mitral  and 
tricuspid  curtains,  so  that  they  close,  by  the  end  of  diastole,  their 
respective  orifices.  Meanwhile  the  semilunar  valves,  kept  tightly 
closed  by  the  high  arterial  pressure,  prevent  leakage  of  blood  from 
the  aorta  and  pulmonary  artery. 

The  "ventricular  systole  now  occurs,  and  the  blood  contained  in  the 
ventricles  is  pumped  forward  into  the  aorta  and  pulmonary  artery, 
whose  semilunar  cusps  are  simultaneously  forced  open  as  soon  as  the 
pressure  in  the  ventricles  exceeds  that  in  the  arteries,  this  change  of 
tension  taking  place  immediately  after  the  ventricles  commence  to 
contract.  Regurgitation  into  the  auricles  cannot  occur  because  the 
mitral  and  tricuspid  valves,  already  approximated  by  the  pressure 
of  the  blood  distending  the  ventricles,  are  kept  tightly  closed  by  the 
impact  of  the  reflux  current  excited  by  the  contraction  of  these 
chambers.  The  contraction  of  the  papillary  muscles  not  only  aids 
in  perfectly  apposing  the  margins  of  the  cusps,  but  also  prevents 
the  eversion  of  the  valves  into  the  auricles.  The  aortic  blood-column 
courses  through  all  parts  of  the  body,  after  which  it  is  returned,  by 
the  venae  cavae,  to  the  right  auricle,  this  complete  circuit  from  the 
left  ventricle  to  the  right  auricle  being  known  as  the  systemic  or 
greater  circulation.  The  blood  in  the  pulmonary  artery  is  propelled 
through  the  lungs,  whence  it  flows  back,  oxygenated,  through  the 
pulmonary  veins,  into  the  left  auricle,  this  short  circuit  being  termed 
the  pulmonary  or  lesser  circulation. 

During  auricular  diastole  the  blood  returns  from  these  two  circuits, 
for  at  this  period  of  the  heart's  cycle  the  pressure  in  the  venae  cavae 
and  pulmonary  veins  exceeds  that  in  the  auricles.  The  latter  are 
distended  by  the  volume  of  their  contained  blood,  aided  to  some 
extent  by  the  elastic  traction  exerted  by  the  lungs,  the  auriculo- 
ventricular  openings  meanwhile  remaining  closed. 

Arterial  Tension. — The  term  blood-pressure  designates  the 
mural  tension  of  the  blood-vessels  exerted  by  the  lateral  and  radial 

lrThe  pressure  in  the  ventricles,  which  at  this  time  are  in  diastole,  is  also 
much  lower  than  in  the  veins,  being  so  low,  indeed,  that  it  is  believed  to  exert 
a  so-called  "suction  action"  upon  the  entering  blood-stream. 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       315 

force  of  the  circulating  blood-stream,  the  degree  of  this  pressure 
varying  in  different  parts  of  the  vascular  path,  according  to  their 
proximity  to  the  heart.  In  this  central  pump  the  pressure  reaches 
the  maximum,  in  the  arteries  it  diminishes,  in  the  capillaries  it 
becomes  still  lower,  and  in  the  veins  it  falls  to  a  minimum;  in  conse- 
quence of  these  differences  the  blood-stream  courses  uninterruptedly 
through  the  body  from  its  ventricular  high-pressure  outlets  at  the 
aortic  and  pulmonary  orifices  to  its  auricular  low-pressure  inlets 
at  the  mouths  of  the  cavae  and  pulmonary  veins.  In  the  venous 
channels  the  blood  is  impelled  heartward  by  three  factors:  the 
initial  cardiac  force,  the  aspiration  action  of  the  heart  and  thorax, 
and  the  pressure  exerted  by  the  body  musculature  upon  the  valvular 
parts  of  the  veins. 

Arterial  tension  is  maintained  by  the  pumping  force  of  the  ven- 
tricles and  by  the  peripheral  resistance,  and  so  long  as  these  two  factors 
work  so  as  to  equalize  the  vascular  outflow  and  inflow  of  blood,  the 
normal  equilibrium  of  pressure  remains  undisturbed.  The  vaso- 
motor  system  of  nerves,  aside  from  regulating  the  distribution  of  the 
blood-mass,  is  a  most  important  factor  in  determining  the  height  of 
the  blood-pressure.  Stimulation  of  the  vasoconstrictors  contracts 
the  peripheral  arterioles,  and  in  so  doing  increases  peripheral  resis- 
tance, thereby  raising  arterial  tension;  paralysis  or  extreme  exhaustion 
of  the  constrictors  has  an  opposite  effect.  Stimulation  of  the  vaso- 
dilator nerves,  by  dilating  the  arteriolar  caliber  and  diminishing 
peripheral  resistance,  lowers  arterial  tension — a  condition,  it  may 
be  added,  much  more  readily  induced  than  increased  tension,  owing 
to  the  relatively  greater  susceptibility  of  the  vasodilators  to  stimulating 
influences. 

The  acme  of  hypertension  develops  when  a  powerful,  overacting 
heart  impels  the  blood-column  against  the  undue  resistance  excited 
by  tight  vasomotor  constriction,  while  the  lowest  degree  of  tension 
is  found  when  a  feeble,  toneless  heart  is  linked  with  the  minimized 
resistance  resulting  from  extreme  vasomotor  dilatation. 

INSPECTION  AND  PALPATION 

It  is  convenient  to  discuss  inspection  and  palpation  of  the  cardio- 
vascular apparatus  together,  rather  than  to  make  an  artificial  division 
of  this  dual  method  of  research.  The  examiner  should  invariably 
preface  his  investigation  of  the  precordial  region  by  a  careful  inspec- 
tion of  the  subject's  facies,  skin,  and  subcutaneous  tissues,  general 
nutrition,  thoracic  configuration,  and  respiratory  movements.  This 


316  PHYSICAL    DIAGNOSIS 

preliminary  inquiry,  the  details  of  which  have  been  considered 
elsewhere  (p.  77  et  seq.),  is  primarily  directed  toward  the  discovery 
of  the  more  general  objective  symptoms  of  heart  disease — pallor, 
cyanosis,  and  icterus;  clubbing  of  the  fingers,  coldness  of  the  extremi- 
ties, venous  tortuosity,  and  edema;  and  polypnea,  dyspnea,  and 
other  forms  of  respiratory  distress.  Advanced  disease  of  the  mitral 
valve,  for  example,  is  suggested  at  first  glance  by  the  pasty,  puffy, 
dusky  face,  the  clubbed,  cold  fingers,  and  the  panting  respiration 
of  the  subject;  coronary  artery  obstruction  and  aortic  arterioscle- 
rosis by  a  dull,  ashen  pallor — the  "leaden  overcast"  of  Sansom; 
while  the  association  of  violent  arterial  throbbing,  urgent  dysp- 
nea, and  an  apprehensive  facies,  by  turn  pallid  and  flushed,  spells 
Corrigan's  disease  to  the  trained  eye. 

More  definite  information  relating  to  the  condition  of  the  heart 
and  blood-vessels  is  obtained  by  further  inquiry,  which  should  in- 
clude the  study  of  the  precordial  contour,  the  apex-beat,  the  presence 
or  absence  of  unnatural  pulsation  and  retraction,  and  the  questions 
of  thrills  and  friction  fremitus.  In  looking  for  obscure  pulsations  and 
irregularities  of  contour  it  often  proves  most  helpful  to  resort  to 
K.  H.  Beall's  device  of  drawing  with  a  skin  pencil,  upon  the  sur- 
face under  investigation,  a  plaid  figure  composed  of  one-inch 
(2.5  cm.)  squares,  whose  lines  become  obviously  distorted  by  surface 
movements  and  irregularities  not  otherwise  perceptible. 

Semirecumbency  is  the  best  position  for  the  subject  to  assume 
during  routine  inspection  and  palpation  of  the  heart  and  great 
vessels,  but  it  is  frequently  advisable  to  test  the  effect  of  gravity  upon 
certain  signs  (pulsations,  thrills,  and  tactile  fremitus),  by  employing 
alternately  the  upright  and  the  recumbent  positions. 

The  influence  of  bodily  posture  upon  cardiac  physical  signs  has 
been  succinctly  summed  up  by  William  Gordon,  who  states  that  a 
change  from  the  erect  to  the  recumbent  position:  (a)  raises  and 
narrows  the  normal  cardiac  dulness;  (6)  greatly  narrows  the  dul- 
ness  of  an  enlarged  heart;  (c)  dulls  the  first,  and  sharpens  the 
second,  cardiac  sound;  (d)  exaggerates  an  accentuated  pulmonic 
second  sound  and  a  reduplicated  second  sound;  (e)  intensifies 
hemic,  mitral  and  tricuspid  regurgitant,  and  aortic  stenotic  mur- 
murs; (/)  enfeebles  the  venous  hum  and  the  mitral  stenotic  bruit; 
and  (g)  leaves  unaltered  the  murmur  of  aortic  regurgitation. 

The  Precordial  Contour. — Bulging  of  the  precordia,  disturbing 
the  normal  bilateral  symmetry  of  the  anterior  chest-wall,  is  much 
more  likely  to  occur  in  children  than  in  adults,  in  consequence  of 
the  greater  resiliency  of  the  parietes  during  immaturity,  and  their 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       317 

readiness  to  yield  to  intrathoracic  pressure.  (See  Fig.  40,  p.  89.) 
A  prominent  precordial  region  suggests  pericardial  effusion,  enlarged 
heart,  circumscribed  pleura!  effusion,  mediastinal  tumor,  or  aneurism 
of  the  aortic  arch,  whereby  the  surface  of  the  chest  is  mechanically, 
if  not  erosively,  made  to  protrude  outward.  Less  commonly,  the 
deformity  is  traceable  to  some  factor  such  as  rickets,  anterolateral 
spinal  curvature,  or  inflammatory  thickening  of  the  surface  structures. 

Precordial  flattening  or  depression,  either  general  or  local,  may 
signify  pericardial  adhesions,  in  which  event  the  change  usually  is 
best  defined  in  the  lower  left  parasternal  area.  Flattening  of  the 
precordia  is  also  referable  to  left-sided  pleural  adhesions  and  to 
fibroid  retraction  of  the  left  lung.  The  depression  of  the  lower 
sternal  region  typical  of  the  "funnel  chest,"  the  mesial  sternal  furrow 
of  the  "gutter  chest,"  and  the  sunken  breast-bone  of  the  "boat- 
shaped  thorax"  have  been  referred  to  under  Examination  of  the 
Thorax.  (See  p.  83.) 

The  Apex-beat. — In  the  healthy  adult  the  apex-beat  of  the  heart 
is  recognized  as  a  rhythmic  local  pulsation  in  the  fifth  left  intercostal 
space,  half  an  inch  (1.25  cm.)  internal  to  the  midclavicular  line,  or 
3^  inches  (8.75  cm.)  external  to  the  midsternal  line.  In  young 
children  the  apex  is  commonly  observed  in  the  fourth  interspace, 
and  as  far  outward  as  the  left  midclavicular  line;  in  short-chested 
subjects  it  may  be  similarly  elevated;  and  in  persons  of  advanced 
age  and  in  those  having  a  long  chest  it  may  beat  at  an  unnaturally 
low  level.  The  word  bathycardia  has  been  proposed  by  E.  J.  Jane- 
way  to  signify  a  low  position  of  the  heart  due  to  physiologic  causes. 

The  apical  pulsation  is  systolic  in  time,  being  synchronous 
with  ventricular  systole,  and  is  ordinarily  restricted  to  an  area  not 
more  than  an  inch  (2.5  cm.)  in  diameter.  In  health  the  right  ven- 
tricle is  to  be  regarded  as  the  clinical  apex  of  the  heart,  and  to  the 
systolic  impact  of  this  chamber  against  the  inner  thoracic  wall  the 
surface  pulsation  is  due;  the  left  ventricle,  which  is  the  anatomic  apex 
of  the  heart,  does  not,  unless  enlarged,  directly  produce  an  appre- 
ciable pulsation  of  the  overlying  parietes.  Usually  the  apex-beat 
can  be  both  seen  and  felt,  but  it  is  by  no  means  rare  to  find  it  invisi- 
ble, though  it  is  distinctly  palpable  as  a  gentle,  pushing  thrust  appreci- 
ated by  the  finger-tip  applied  to  the  apex  region.  Deep  inspiration 
slightly  depresses,  and  forced  expiration  elevates,  the  site  of  the  apex, 
which  also  shifts  horizontally  when  the  subject  turns  from  dorsal  to 
lateral  recumbency,  the  deflection  amounting  to  an  inch  or  two  to- 
ward the  left  when  left  lateral  decubitus  is  assumed.  Postural 


318  PHYSICAL  DIAGNOSIS 

mobility  of  the  apex,  which  is  greater  in  adults  than  in  children, 
is  especially  apparent  in  subjects  of  cardiovascular  disease. 

Having  identified  the  apex-beat,  it  is  necessary  to  learn  whether 
the  impulse  is  situated  normally  or  displaced,  whether  its  force  is 
exaggerated  or  enfeebled,  and  whether  the  area  of  pulsation  is 
diminished  or  extended.  These  points  are  decided  by  combined 
inspection  and  palpation  of  the  precordial  region. 

Displacement  of  the  Apex-beat. — Of  the  numerous  factors  of  apical 
displacement,  the  most  important  relate  to  enlargement  of  the  heart 
by  hypertrophy  and  dilatation,  to  dislocation  of  the  organ  by  intra- 
thoracic  traction  or  pressure  and  by  ascent  of  the  diaphragm,  and 
to  the  collection  of  fluid  within  the  pericardial  sac.  Aside  from  these 
causes,  the  effect  of  thoracic  deformities  and  of  visceral  transposition 
on  the  site  of  the  apex-beat  is  also  to  be  recalled. 

Upward  apical  displacement  may  indicate  unduly  great  subphrenic 
pressure,  in  consequence  of  which  the  diaphragm,  and  with  it  the 
heart,  rises  to  a  high  level,  as  in  ascites,  meteorism,  gastric  distention, 
and  abdominal  tumor;  diaphragmatic  hernia  also  may  elevate  the 
heart's  impulse.  Upward  displacement,  with  more  or  less  deviation 
of  the  apex  to  the  left,  occurs  from  effusion  of  fluid  or  of  gas  in  the 
right  pleural  sac,  adhesions  of  the  left  pleura  and  fibrosis  of  the 
corresponding  lung,  large  pericardial  effusion,  and  mediastinal 
neoplasm.  A  heart  that  has  undergone  considerable  atrophy 
obviously  is  likely  to  pulsate  at  too  high  a  site. 

Downward  apical  displacement  ordinarily  is  referable  to  pressure 
exerted  by  hypertrophic  emphysema;  less  commonly  the  weight  of  an 
aortic  aneurism  or  of  a  mediastinal  tumor  depresses  the  apex;  or  it 
may  be  dragged  downward  by  an  enlarged  liver  or  by  some  form  of 
visceral  ptosis. 

Right  lateral  apical  displacement  is  generally  attributable  to  such 
lesions  as  right-sided  pulmonary  fibrosis  and  pleuropericardial 
adhesions;  to  collapse  of  the  right  lung;  and  to  the  pressure  of  a  left- 
sided  pleural  effusion  or  pulmonary  consolidation.  In  congenital 
transposition  of  the  viscera  the  apex-beat  is  to  be  looked  for  at  a 
point  in  the  fifth  right  interspace,  near  the  midclavicular  line — a 
condition  of  dextrocardia  giving  the  so-called  "mirror  image"  of  the 
precordial  and  other  regions. 

Left  lateral  apical  displacement,  if  practically  horizontal,  is  espe- 
cially significant  of  dilated  hypertrophy  of  the  right  ventricle,  whose 
strong  epigastric  and  parasternal  pulsations  must  not  be  mistaken 
for  its  actual  apical  impulse.  The  apex  beats  to  the  left  of,  and 
below,  its  normal  situation  in  dilated  hypertrophy  of  the  left  ventricle. 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       319 

The  character  of  the  apex-beat  as  to  force,  extent,  and  rhythm 
varies  both  in  health  and  in  disease,  so  that  should  such  deviations 
from  normal  be  found,  it  is  necessary  first  to  determine  if  they  are 
physiologic  or  pathologic,  and,  if  the  latter,  to  discover  the  lesion, 
cardiac  or  extracardiac,  upon  which  they  depend.  In  judging  the 
force  of  the  apex-beat,  allowance  is  to  be  made  for  the  facts  that  a 
thin  chest-wall  magnifies,  and  a  thick  chest-wall  minimizes,  the 
impulse;  and  that  should  the  impact  of  the  ventricle  be  directed 
against  a  rib  rather  than  an  interspace,  the  apex-beat  naturally  will 
be  indefinable  by  inspection  and  palpation.  The  apex-beat  may 
also  be  absent  in  an  individual  whose  thorax  is  so  deep  that  the 
heart  fails  to  impinge  against  the  inner  thoracic  wall. 

Simple  exaggeration  of  the  force  of  the  apical  impulse  may  be  due 
to  nervous  excitement,  overexercise,  indigestion,  anemia,  and  the 
overuse  of  tobacco,  coffee,  tea,  and  alcohol.  The  "fluttering" 
of  the  heart  complained  of  by  the  neurotic  woman,  and  the  precordial 
throbbing  of  the  indiscreet  coffee-drinker  and  smoker,  are  familiar 
illustrations  of  this  type  of  apex  overaction.  It  may  accompany 
acute  myocarditis,  valvular  disease,  and  left  ventricular  hypertrophy — 
in  the  last-named  lesion  the  impact  is  not  only  forcibly  heaving,  but 
diffuse  and  displaced  downward  and  to  the  left.  Forcible  throbbing 
of  the  apex  attends  the  initial  stages  of  many  acute  febrile  dis- 
eases, and  is  seen  in  apoplexy.  An  apparently  exaggerated  apex- 
beat  may  be  due  to  retraction  of  the  left  lung,  whereby  the  heart 
is  uncovered  and  hence  pulsates  against  the  chest-wall  more  forcibly 
and  more  extensively  than  in  health. 

An  enfeebled  or  absent  apex-beat  should  always  arouse  one's  sus- 
picion of  cardiac  dilatation,  the  relaxed  ventricle  either  quite  oblitera- 
ting the  impulse,  or  rendering  it  feeble,  undulatory,  and  of  a  distinc- 
tively "slapping"  character.  The  slow,  deliberate  systole  of  the 
left  ventricle  commonly  associated  with  aortic  stenosis  may  be  so 
forceless  as  to  give  rise  to  no  appreciable  impulse  in  the  region  of  the 
apex.  Pericardial  effusion,  emphysema,  and  mediastinopericardial 
adhesions  also  are  capable  of  weakening  or  negativing  the  apical 
beat — pericardial  effusion,  by  interposing  a  barrier  of  fluid  between 
the  heart  and  the  thoracic  wall;  emphysema,  by  hemming  in  the 
whole  anterior  surface  of  the  heart  with  a  mass  of  overdistended 
lung  tissue;  and  mediastinopericardial  adhesions,  by  mechanically 
restricting  the  heart's  excursions  by  the  contraction  of  the  fibrous 
bands  by  which  the  organ  is  anchored.  Advanced  myocarditis, 
myocardial  degeneration,  cardiac  atrophy,  and  systemic  shock  and 
debility  materially  lessen  the  force  of  the  apex-beat.  Exceptionally, 


320 


PHYSICAL   DIAGNOSIS 


every  trace  of  the  precordial  impulse  is  obliterated  by  either  a 
neoplasm  or  an  inflammatory  lesion  of  the  anterior  mediastinum, 
whereby  the  heart  is  pushed  backward  and  its  throbs  are  com- 
pletely damped. 

The  cardiogram  of  the  apex-beat  (Fig.  124;  cf.  Fig.  14)  may 
show  unnatural  deviations  that  serve,  within  reasonable  limits,  as 
criteria  of  disturbances  affecting  the  rate,  force,  and  rhythm  of  the 


::: 


::!:^^ 


Fig.  124. — Normal  cardiogram  of  the  apex- beat:  a,  Auricular  systole;  a-b, 
upstroke  (systole);  b,  apex;  b-c-d,  systolic  plateau  (cardiac  impact);  d-e,  downstroke 
(diastole);  d,  aortic  valve  closure;  e-f-a,  ventricular  filling.  (Tracing  by  Dr.  G. 
Bachmann.) 

heart,  more  especially  when  interpreted  in  the  light  of  simultaneous 
tracings  of  the  radial  and  jugular  pulsations.  The  cardiographic 
upstroke  is,  unfortunately,  no  certain  index  to  the  force  of  the  ven- 
tricular systole,  since  a  sudden,  sharp  impact  of  the  heart,  though 
the  actual  force  be  subnormal,  may  produce  quite  as  high  a  rise  as 
that  due  to  a  powerful  contraction.  Uneven  spacing  of  the  upstroke 
intervals,  if  instrumental  defects  can  be  excluded,  means  ventricular 
arhythmia.  The  apex,  if  sharply  acute,  denotes  rapid  emptying  of 
the  ventricle,  as  the  result,  for  example,  of  the  double  ventricular 
outlet  established  by  fault  of  a  mitral  insufficiency;  an  obtuse,  blunt 
apex  indicates  an  opposite  state  of  things,  as  in  aortic  stenosis.  The 
systolic  plateau  corresponds  in  length  to  the  duration  of  ventricular 
systole,  and  an  unduly  broad  and  horizontal  wave  in  this  situation 
suggests  the  deliberate  systoles  which  accompany  many  cases  of 
aortic  stenosis.  The  downstroke,  being  related  to  diastole,  follows 
a  course  the  obliquity  of  which  increases  in  correspondence  with  the 
prolongation  of  this  phase.  The  diastolic  rise  ascends  as  a  short, 
steep  curve  when  diastole  is  sharp  and  sudden,  but  mounts  gradually 
upward  when  the  diastolic  relaxation  is  prolonged.  Vertical  oscilla- 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM        321 


tions  of  the  base  line,  it  should  be  also  noted,  are  explained  chiefly 
by  disturbances  in  the  waves  of  the  diastolic  rise  and  fall  between 
the  systolic  plateau  and  upstroke. 

Abnormal  Areas  of  Pulsation  (Fig.  125). — Apart  from  pulsations 
directly  referable  to  the  apical  thrust,  those  occurring  in  other  parts 
of  the  precordia  and  in  regions  of  the  thorax  adjacent  thereto  remain 
to  be  identified  and  interpreted  in  an  etiologic  light.  Such  anomalies 


Right  ventricle 


Liver 


Jugular 
Innominate;   aorta 

Conus  arteriosus 
Pulsating  pleurisy 

Right  ventricle 
Aorta;  right  ventricle 
Left  ventricle 
Aorta 


Pulsations 

Visceral 
Fig.  125. — Areas  of  abnormal  pulsation. 

arise  chiefly  from  lesions  of  the  heart  and  large  vascular  channels, 
but  they  may  also  be  due  in  many  instances  to  a  conduction  of  the 
normal  cardiac  and  arterial  impact  by  the  medium  of  neighboring 
morbid  structures.  Like  the  apex-beat,  these  pulsations  are  often 
both  visible  and  palpable,  though  some  are  palpable  only;  unlike 
the  apex-beat,  an  extra-apical  pulsation  may  have  a  distinctly  expan- 
sile character  and  may  be  found  over  a  local  tumor  upon  the  surface 
of  the  chest.  Pulsations  of  cardiac  origin  are  typically  systolic  in 


322  PHYSICAL    DIAGNOSIS 

time,  but  those  of  arterial  and  venous  nature  vary  in  time-incidence 
according  to  the  mechanism  whereby  they  are  produced.  The 
neck,  the  area  corresponding  to  the  base  of  the  heart,  the  precordia 
and  its  vicinity,  the  epigastrium,  and  the  region  of  the  liver  all  should 
be  examined  for  evidences  of  abnormal  throbbing,  whose  rhythm 
is  determined  by  comparison  with  the  apex-beat. 

Pulsations  on  either  side  of  the  neck  may  originate  in  the  carotid 
artery  or  in  the  jugular  vein.  If  carotid,  it  is  recognized  as  a  systolic 
throbbing  along  the  course  of  the  vessel  from  the  sternoclavicular 
articulation  to  a  midpoint  between  the  angle  of  the  jaw  and  the 
mastoid  process.  Pulsation  in  this  site  is  due  to  much  the  same 
factors  that  account  for  a  tumultuous  apex-beat — neurotic  influ- 
ences, overexertion,  and  the  abuse  of  tobacco  and  other  heart  irri- 
tants. Carotid  pulsation  is  especially  significant  of  left  ventricular 
hypertrophy,  with  or  without  aortic  leakage;  of  aneurism  of  the 
aortic  arch;  of  exophthalmic  goiter;  of  advanced  arterial  sclerosis; 
of  cerebral  hemorrhage;  and  of  high-grade  anemia.  In  rare  in- 
stances the  cause  has  been  found  to  be  an  obliterative  endarteritis 
of  the  descending  portion  of  the  aortic  arch.  Local  expansile  pul- 
sation of  a  common  or  an  external  carotid  artery  may  be  due  to  a 
small  aneurismal  dilatation  of  the  vessel. 

Pulsation  of  the  jugular  veins,  which  is  always  more  marked  on 
the  right  side,  is  recognized  as  a  throbbing  along  the  course  of  these 
vessels  upward  over  the  clavicular  belly  of  the  sternocleidomastoid 
muscles.  It  is  of  the  greatest  importance  to  determine  whether 
these  pulsations  are  systolic,  presystolic,  or  both.  Systolic  jugular 
pulsation  is  almost  proof  positive  of  tricuspid  valve  leakage,  and 
indicates  a  ventricular,  or  positive  type  of  venous  pulse;  presystolic 
jugular  pulsation  is  not  necessarily  pathologic,  and  means  an  auric- 
ular, or  negative,  variety  of  venous  pulse.  Very  exceptionally,  it 
is  possible  to  assign  a  factor  other  than  tricuspid  leakage  to  a  systolic 
venous  pulse,  as,  for  example,  aneurism  implicating  the  superior 
cava,  and  also  mitral  regurgitation  plus  patent  foramen  ovale,  both 
of  which  defects  favor  transmission  of  the  ventricular  impact  through 
the  venous  columns  emptying  into  the  right  heart.  The  differentia- 
tion and  clinical  significance  of  these  two  kinds  of  jugular  pulsation 
are  considered  under  the  Venous  Pulse.  (See  p.  346.) 

Ordinarily,  the  venous  pulse  is  observed  only  in  the  jugulars, 
but  in  extreme  cases  it  may  penetrate  their  smaller  surface  tribu- 
taries and  extend  to  other  extremital  veins.  The  palpable  hepatic 
pulse,  described  below,  shows  the  extent  to  which  the  ventricular 
beats  sometimes  regurgitate  through  the  veins. 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM        323 

Diastolic  collapse  of  the  jugulars  (Friedreich's  sign)  occurs  with 
frequency  in  chronic  adhesive  pericarditis;  it  has  been  attributed 
to  a  sudden  emptying  of  these  veins  at  the  time  of  diastole,  which 
allows  the  chest-wall,  tightly  drawn  in  by  adhesions  during  systole, 
suddenly  to  relax  and  expand,  and  thus  to  exert  an  aspiratory  action. 
Collapse  of  a  jugular  vein,  if  permanent  despite  pressure  centrally 
applied,  is  significant  of  thrombosis  of  the  lateral  sinus. 

Pulsation  in  the  episternal  notch  may  not  be  abnormal  in  the 
emaciated  and  in  the  aged,  and  it  also  may  arise  as  the  result  of  neu- 
roses, anemia,  and  indulgence  in  stimulants.  Other  causes  of  a  systolic 
pulsation  in  this  area  are  dilatation  of  the  transverse  portion  of  the 
aortic  arch,  usually  aneurismal;  aneurism  of  the  innominate  artery; 
and  exposure  of  the  right  subclavian  artery  by  a  contracted  lung 
or  conduction  of  its  pulsation  by  a  consolidated  lung  of  the  corres- 
ponding side.  The  existence  of  cervical  ribs,  and  anomalies  in  the 
size  and  distribution  of  the  vessels  at  the  root  of  the  neck  are  also 
among  the  possible  causes  of  a  systolic  throb  in  this  region. 

Pulsation  at  or  near  the  base  of  the  heart,  if  not  due  simply  to  violent 
cardiac  overaction,  may  mean  aneurism  of  the  aortic  arch,  or  dilata- 
tion of  the  arch  in  consequence  of  atheroma  or  of  Corrigan's  dis- 
ease. Systolic  throbbing  in  the  first  or  second  right  intercostal  spaces 
near  the  sternal  border  is  produced  by  aneurism  of  the  ascending 
portion  of  the  aortic  arch;  over  the  angle  of  Louis,  at  the  level  of  the 
second  rib,  by  aneurism  of  the  transverse  portion;  and  in  the  second 
or  third  left  interspaces,  by  aneurism  of  the  descending  portion. 
Aneurismal  throbbing  in  these  sites,  when  typical,  is  attended  by  a 
distinct  diastolic  shock,  and  should  it  occur  over  a  circumscribed 
bulging  of  the  chest  wall,  has  an  expansile  character.  The  impulse 
of  the  conus  arteriosus  of  the  right  ventricle  may  account  for  a 
systolic  pulsation  near  the  left  sternal  edge  as  high  up  as  the  second 
interspace.  Diastolic  pulsation  in  the  second  left  interspace  near 
the  sternal  border  is  a  common  early  sign  of  incipient  pericarditis. 
Pulsation  between  the  right  sternal  and  midclavicular  lines  and 
between  the  second  and  fourth  interspaces  is  sometimes  due  to 
displacement  of  the  heart  by  the  traction  of  a  fibroid  right  lung,  or 
by  the  pressure  of  left-sided  pleural  effusion,  pneumothorax,  or 
neoplasm. 

Pulsation  in  the  precordial  area  in  the  third,  fourth,  or  fifth  inter- 
spaces at  the  right  sternal  border  may  be  caused  by  cardiac  dislocation 
from  any  of  the  factors  just  mentioned,  but  it  also  commonly  results 
from  right  auricular  dilatation.  An  hypertrophied  and  dilated  right 
ventricle  may  be  the  factor  of  throbbing  immediately  alongside  the 


324  PHYSICAL    DIAGNOSIS 

left  sternal  border,  between  the  third  and  sixth  interspaces  inclusive. 
Pulsating  pleurisy,  usually  purulent,  sometimes  produces  a  throbbing 
or  an  undulation  of  one  or  several  interspaces,  almost  invariably 
on  the  left  side,  between  the  second  and  sixth  ribs,  and  between  the 
left  border  of  the  precordia  and  the  axilla. 

Pulsation  in  the  epigastrium  depends  upon  a  number  of  different 
factors,  referable  in  the  main  to  the  heart,  the  gut,  and  the  viscera 
of  the  upper  abdominal  zone.  Systolic  epigastric  throbbing  may  be 
due  simply  to  overaction  of  the  heart,  or  to  congenital  shortness  of 
the  sternum,  owing  to  which  the  anterior  surface  of  the  right  ventricle 
beats  against  the  soft  structures  of  the  epigastrium,  rather  than 
against  bone.  The  same  sign  may  indicate  right  ventricular  hyper- 
trophy and  dilatation,  or  a  displacement  of  the  heart  to  the  right  by 
one  of  the  causes  enumerated  above.  Postsystolic  pulsations  originate 
in  the  abdominal  aorta,  commonly  as  the  result  of  the  so-called 
dynamic  pulsation  of  this  vessel,  such  as  is  encountered  in  neurasthenia 
and  in  severe  anemia.  Aneurism  of  the  abdominal  aorta,  enlarged 
peritoneal  lymphatics,  tumors  of  the  liver,  stomach,  gut,  and  pan- 
creas, as  well  as  tightly  impacted  fecal  masses  overlying  the  aorta, 
all  may  transmit  the  throb  of  this  artery  as  an  epigastric  pulsation 
occurring  a  trifle  later  than  the  ventricular  systole. 

Pulsation  of  the  liver  is  practically  a  pathognomonic  sign  of  tri- 
cuspid  regurgitation,  though  its  occurrence  in  connection  with  this 
lesion  is  by  no  means  constant.  The  throb  of  a  pulsating  liver  is 
felt  in  the  right  hypochondrium  (not  merely  in  the  epigastrium), 
below  the  lower  costal  border,  and  is  most  readily  detected 
by  bimanual  palpation.  The  time  of  such  a  pulsation  is  tardily 
systolic,  and  its  character  is  expansile — not  merely  a  lifting  thrust, 
like  that  of  a  liver  jogged  by  a  forcible  heart-beat;  it  reflects  the 
heart's  impulse  communicated,  by  fault  of  a  leaky  tricuspid  orifice, 
through  the  inferior  vena  cava  to  the  hepatic  veins,  with  a  conse- 
quent rhythmic  distention  of  the  liver  directly  after  systole. 

Abnormal  Areas  of  Retraction. — Broadbent's  sign,  or  a  systolic 
retraction  of  the  tenth  and  eleventh  intercostal  spaces  below  the 
left  scapula,  sometimes  attended  by  a  synchronous  tug  upon  the 
eleventh  and  twelfth  ribs,  was  first  described  by  the  younger 
Broadbent  as  an  indication  of  chronic  adhesive  pericarditis,  in 
which  condition  the  diaphragm,  anchored  by  dense  adhesions  to 
the  pericardium,  is  dragged  upward  with  each  systole  of  the  hyper- 
trophied  heart,  so  that  the  diaphragmatic  attachments  to  the  chest- 
wall  are  pulled  inward  and  retracted  (Fig.  126).  This  sign  must 
be  carefully  distinguished  from  a  similar  systolic  retraction  due  to 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       325 

the  tug  of  an  hypertrophied  or  a  greatly  overacting  heart,  and  met 
with  especially  in  emaciated  subjects,  as  Tallant  has  shown. 
Broadbent's  sign  is  commonly  attended  by  systolic  retraction  of 
the  seventh  and  eighth  ribs  and  intervening  interspace  near  the 
left  parasternal  line,  by  systolic  dimpling  in  the  region  of  the  apex, 
and  by  respiratory  immobility  of  the  epigastrium. 

In  aortic  regurgitation  a  systolic  retraction  over  the  precordia,  due 
to  atmospheric  pressure,  is  sometimes  demonstrable;  and  in  some 
cases  of  mitral  stenosis  a  late  diastolic  retraction  is  visible  in  the 


Fig.  126. — Local  systolic  retractions  of  the  thorax  due  to  adherent  pericardium. 

same  situation.  Recessions  of  this  sort,  which  are  due  simply  to 
sudden  depression  of  the  parietes  provoked  by  strong  pulsation,  are 
to  be  discriminated  from  the  cardiac  tug  exerted  upon  the  chest- 
wall  by  an  adherent  pericardium. 

Venous  Engorgement.— Circumscribed  venous  engorgements  arise 
in  consequence  of  local  interference  with  the  venous  current,  the 
stasis  thus  established  being  shown  by  the  distended,  tortuous  con- 
dition of  the  superficial  veins  draining  the  area  peripheral  to  the 
point  of  obstruction.  The  undue  prominence  of  the  surface  veins 
and  their  tendency  to  form  anastomoses  upon  the  anterior  thoracic 
wall  in  cases  of  mediastinal  tumor  (Fig.  50),  and  the  abnormal  size 
of  a  venous  trunk  distal  to  a  thrombotic  obstruction,  are  exam- 


326  PHYSICAL   DIAGNOSIS 

pies  of  the  changes  wrought  by  local  obstructions  to  the  venous 
circulation. 

Engorgement  of  the  jugular  veins  occurs  as  a  physiologic  respiratory 
phenomenon  and  as  the  result  of  pathologic  interference  with  the 
venous  return  flow  into  the  right  auricle.  The  normal  inspiratory 
acceleration  and  expiratory  delay  in  the  venous  current  can  be 
demonstrated  by  inspection  of  the  external  jugular  veins  while  the 
subject  breathes  forcibly  and  deeply,  from  the  effects  of  which  the 
jugulars  become  appreciably  fuller  during  expiration,  or  the  period 
of  normal  venous  retardation.  The  vascular  stress  incident  to  chronic 
cough  and  dyspnea  exaggerates  this  respiratory  phenomenon  and  ulti- 
mately creates  permanent  distention  of  the  jugulars,  as  in  asthma, 


Fig.  127. — Jugular  engorgement  (Jefferson  Hospital). 

emphysema,  and  other  chronic  affections  of  the  bronchopulmonary 
structures.  Inspiratory  overfulness  of  these  veins — the  reverse  of  their 
normal  state — may  accompany  mediastinopericarditis  and  medias- 
tinal  tumor,  indicating  compression  or  traction  of  the  intrathoracic 
venous  trunks  (Kussmaul's  sign).  Habitual  jugular  enlargement 
from  lesions  that  obstruct  the  flow  through  the  veins  into  the  heart, 
suggests,  if  bilateral,  cardiac  dilatation  or  compression  of  the  superior 
cava,  the  innominate  or  the  jugular  veins  by  aneurism  or  by  medi- 
astinal  tumor;  if  unilateral,  the  sign  points  to  compression  of  one 
innominate  or  jugular  vein,  as  by  a  neoplasm  or  by  an  enlarged 
gland. 


EXAMINATION   OF    THE    CARDIOVASCULAR    SYSTEM       327 

Enlargement  and  tortuosity  of  other  superficial  veins — notably, 
those  of  the  upper  thorax  and  the  arms,  the  costal  arch,  and  the 
upper  part  of  the  abdomen — have  been  specially  dealt  with  else- 
where. (See  pp.  105,  106.) 

General  venous  engorgement,  ultimately  attended  by  edema  of  the 
congested  parts,  points  to  cardiac  enfeeblement  the  precise  character 
and  degree  of  which  are  to  be  determined  by  examining  the  heart, 
especially  the  right  side. 

Thrills. — A  thrill  is  the  tactile  equivalent  of  a  murmur,  and,  like 
the  latter,  has  a  point  of  maximum  intensity  and  a  definite  incidence 
in  relation  to  the  cardiac  cycle.  Thrills  are  excited  by  blood-eddies 
churned  into  vibrations  by  the  same  lesions  that  account  for  the 
production  of  murmurs,  and  are  distinguished  by  the  palpating  hand 
as  a  fine  or  rough  vibration,  somewhat  like  the  purr  of  a  cat — hence 
the  terms,  " f remissement  cataire"  and  " Katzenschiirren."  In 
studying  a  thrill  the  palm  of  the  hand  or  the  finger-tips  should  be 
applied,  with  moderate  pressure,  to  the  surface  of  the  chest,  and  the 
patient  instructed  not  to  breathe  while  the  examiner  times  the  occur- 
rence of  the  sign,  and  notes  its  situation,  extent,  quality,  and  point 
of  greatest  intensity. 

Thrills  at  the  base  of  the  heart  may  be  symptomatic  of  aortic  and 
pulmonary  valvular  defects,  of  aortic  roughening,  dilatation,  and 
aneurism,  and  of  Graves'  disease.  At  the  second  right  intercostal 
space,  close  to  the  sternal  border,  a  systolic  thrill,  often  carried  upward 
into  the  carotids,  is  found  in  aortic  stenosis  and  in  roughened  aorta; 
while  if  diastolic,  and  conducted  down  the  sternum,  a  thrill  in  this 
site  may  denote  aortic  regurgitation.  A  systolic  thrill  in  the  second 
left  interspace  at  the  sternal  edge  occurs  occasionally  in  pulmonary 
stenosis,  and  commonly  in  exophthalmic  goiter;  and  a  diastolic 
thrill  in  the  same  area  may  mean  pulmonary  regurgitation.  Aneu- 
rismal  thrills  may  be  felt  over  the  entire  upper  and  middle  precordia, 
and  usually  also  in  the  arteries  of  the  neck  and  in  the  episternal 
notch;  in  the  latter  depression  the  systolic  thrill  of  a  dilated  aorta 
may  also  be  perceptible. 

Thrills  at  or  near  the  apex  of  the  heart  are  due  generally  to  lesions 
of  the  mitral  valves;  less  commonly  they  are  transmitted  from  the 
base  of  the  heart.  If  systolic,  an  apical  thrill  commonly  indicates 
mitral  regurgitation,  or,  very  rarely,  aortic  stenosis;  if  presystolic, 
it  is  an  almost  certain  sign  of  mitral  stenosis,  much  less  commonly 
being  due  to  a  Flint  murmur  of  Corrigan's  disease  (q.  v.);  if 
diastolic,  it  may  represent  the  conducted  thrill  of  this  last-named 
lesion. 


328  PHYSICAL    DIAGNOSIS 

Thrills  over  the  xiphoid  and  lower  sternal  region,  systolic  in  time, 
can  be  demonstrated  in  many  cases  of  organic  tricuspid  regurgita- 
tion  and  of  dilatation  of  the  tricuspid  orifice.  Tricuspid  stenosis 
sometimes  accounts  for  a  presystolic  thrill  in  this  situation. 

Friction  Fremitus. — Fremitus  due  to  the  rubbing  together  of 
roughened  pericardial  or  pleural  surfaces  is  perceptible  as  a  deli- 
cate crackling  or  coarser  creaking  sensation,  of  a  much  more  cir- 
cumscribed and  superficial  character  than  that  of  a  thrill. 

Pericardial  friction  fremitus  generally  is  distinguished  by  a  to-and- 
fro  rhythm,  which,  however,  bears  no  definite  relation  to  the  heart- 
sounds;  it  is  most  distinctly  felt,  as  a  rule,  between  the  second  and 
fourth  intercostal  spaces,  at  and  near  the  left  sternal  border;  and  it 
is  exaggerated  by  pressure  with  the  palpating  finger  and  by  making 
the  patient  bend  forward.  (See  Fig.  159.) 

Pleuropericardial  friction  gives  rise  to  fremitus  synchronous  with 
the  heart-sounds,  being  especially  well  related  to  the  ventricular 
contractions;  it  is  generally  most  distinct  over  the  area  corresponding 
to  the  tongue  of  lung  overlapping  the  heart  between  the  fourth  and 
sixth  ribs.  According  to  the  pleural  reflection  implicated,  whether 
pulmonary  or  costal,  pleuropericardial  friction  is  palpable  during 
either  inspiration  or  expiration.  (See  Figs.  91  and  92.) 

Tracheal  Tugging. — Compresson  of  the  left  bronchus  by  an 
aortic  aneurism,  and  adhesions  between  an  aneurismal  sac  and  the 
trachea  or  bronchi,  cause  a  slight  descent  of  the  windpipe  with 
each  pulsation  of  the  aorta.  1'his  downward  movement  of  the 
trachea  is  in  turn  transmitted  to  the  larynx,  the  systolic  depression 
of  which  is  appreciated  on  palpation  as  a  distinct  tug  synchronous 
with  cardiac  systole.  Sometimes  this  indication  of  tracheal  tugging 
(Oliver's  sign)  is  visible,  as  well  as  palpable,  and,  exceptionally,  it 
has  a  diastolic  rhythm.  The  sign  is  elicited  by  supporting  and 
elevating  the  cricoid  cartilage  with  the  thumb  and  forefinger,  the 
patient  meanwhile  closing  the  mouth  and  raising  the  chin,  so  as  to 
stretch  the  trachea  and  keep  it  tense.  The  tug  can  also  be  appre- 
ciated by  grasping  and  elevating  the  body  of  the  hyoid  bone  (M. 
L.  Graves). 

Tracheal  tugging,  though  most  suggestive  of  aneurism  of  the 
thoracic  aorta,  cannot  be  regarded  as  pathognomonic,  inasmuch  as 
it  has  been  met  with  in  simple  dilatation  of  the  aortic  arch  and  in 
pulsating  mediastinal  sarcoma.  Actual  downward  traction  of  the 
trachea  is  to  be  distinguished  from  a  spurious  tug  due,  for  instance, 
to  carotid,  thyroid,  or  innominate  pulsation. 

The  Arterial  Pulse. — The  pulse-beat  corresponds  to  the  wave 
of  increased  intra-arterial  pressure  excited  by  ventricular  systole, 


EXAMINATION    OF   THE    CARDIOVASCULAR    SYSTEM       329 

the  tactile  impressions  thereby  afforded  being  due  to  alteration  in 
the  shape  and  increase  in  the  diameter  of  the  artery's  lumen.  Of 
these  changes  the  first,  which  alters  the  vessel's  lumen  from  a  flat 
to  a  circular  shape,  is  the  predominant  factor  of  the  pulse-beat, 
for  the  expansion  of  the  artery  is  too  insignificant  to  be  appreciated 
by  palpating  a  peripheral  vessel,  such  as  the  radial  artery. 

The  normal  pulse  beats  at  the  rate  of  about  70  to  75  a  minute  in 
the  adult  male,  being  somewhat  more  frequent  in  women  and  much 
more  so  in  children.  The  pulsations,  which  follow  a  rhythmic 
sequence,  occur  synchronously  at  both  wrists,  and  are  of  well-sus- 
tained volume  and  moderate  force.  Save  when  the  vessel  is  unusually 
large  and  superficial,  its  structure  cannot  be  felt.  A  clinical  analysis 
of  the  pulse  requires  minute  attention  to  the  following  details:  the 
condition  of  the  arterial  wall  and  the  size  of  the  vessel;  the  pulse-rate, 
rhythm,  tension,  and  volume;  and  the  bilateral  symmetry  of  the 
pulses  and  their  relation  to  cardiac  systole. 

Technic  of  Feeling  the  Pulse. — With  the  patient's  forearm  turned 
in  partial  supination  and  supported  at  the  level  of  the  heart,  the 
first  three  fingers  of  the  examiner's  hand  are  pressed  lightly  against 
the  radial  artery  at  the  wrist.  The  points  to  be  investigated  should 
be  studied  individually  and  with  proper  deliberation,  for  the  feeling  of 
the  pulse  is  not  merely  a  mechanical  act,  but  one  demanding  both 
skill  and  experience  linked  with  a  keen  appreciation  of  cardiovascular 
functions,  normal  and  disordered,  and  the  ability  to  correlate  them 
with  the  tactile  impressions  perceived  at  the  wrist.  The  condition 
of  the  arterial  wall  and  the  size  of  the  artery  are  readily  discovered 
by  simple  palpation  and  by  "fingering"  the  vessel — which  means 
gently  sliding  the  pad  of  the  finger  across  it  transversely  and  along 
its  course  longitudinally,  varying  the  pressure  meanwhile  so  as  to 
roll  the  artery  against  the  bone.  By  these  maneuvers,  changes 
such  as  diminished  elasticity,  tortuosity,  and  mural  irregularities, 
are  made  perfectly  plain.  The  pitlse-rale  is  ordinarily  estimated 
by  counting  the  number  of  beats  felt  during  twenty  seconds  and 
multiplying  them  by  three,  but  when  the  pulse  is  notably  arhythmic, 
slow,  or  fast,  it  is  a  better  plan  to  count  it  for  a  full  minute.  Some 
clinicians  calculate  the  rate  of  an  excessively  rapid  pulse  by  indicating 
each  beat  by  a  lead-pencil  dot,  and  subsequently  counting  the  number 
of  dots  made  during  a  stated  period.  A  general  idea  of  the  rhythm 
of  the  pulse  is  gained  at  the  time  its  rate  is  counted,  and  should 
irregularity  be  found,  the  type  should  be  carefully  identified  by  a 
further  digital  examination,  supplemented,  in  suitable  instances, 
by  sphygmography.  The  arterial  tension  may  be  approximated 
by  noting  the  pressure  required  to  obliterate  the  pulse-beat,  the 


330  PHYSICAL   DIAGNOSIS 

manner  of  obtaining  this  information  consisting  in  gradually  increas- 
ing the  pressure  of  the  proximal  finger  until  the  middle  finger  fails 
to  feel  pulsation,  the  distal  finger  meanwhile  exerting  firm  pressure 
below,  in  order  to  block  peripheral  waves.  The  sphygmomanometer 
must,  of  course,  be  employed  for  accurate  measurements  of  the 
blood-pressure.  (See  p.  31.)  The  -volume  of  the  pulse  is  judged 
by  palpating  with  gentle  pressure,  at  first  uniform  and  then  progres- 
sively increased,  with  a  view  to  ascertaining  the  amount  of  dis- 
tention  that  the  artery  undergoes  with  each  systole  of  the  ventricles. 
The  synchronism  and  comparative  force  of  the  two  radials  are  shown 
by  bilateral  palpation,  while  the  relation  of  the  pulses  to  cardiac 
systole  is  learned  by  simultaneous  radial  and  precordial  palpation. 


Ventricular  systole    Aortic  valve  closure 

Fig.  128. — Sphygmogram  of  the  normal  radial  puke:  a-b,  Upstroke;  b-e,  down- 
stroke;  ft,  apex;  c,  predicrotic  (tidal)  wave;  d,  dicrotic  (recoil)  wave.  (Tracing  by 
Dr.  G.  Bacnmann.) 

Clinical  Significance  of  the  Sphygmogram. — The  following 
details  of  the  radial  Sphygmogram  serve  as  a  basis  for  the  interpreta- 
tion of  various  changes  produced  by  diseases  of  the  cardiovascular 
system  (Fig.  128;  cf.  Fig.  14).  The  special  tracings,  some  of 
which  have  quite  a  distinctive  relation  to  certain  types  of  valvular 
disease  and  cardiac  arhythmia,  are  discussed  in  connection  with 
these  conditions  in  Section  VI. 

The  Course  of  the  Base  Line. — The  substitution  of  a  wavy  base 
line  for  one  which  runs  a  straight  course  is  met  with  in  conditions 
of  dyspnea  and  subnormal  blood-pressure,  the  undulations  rising 
with  expiration  and  falling  with  inspiration. 

The  Angle  of  the  Apex. — A  sharp  apex  with  an  unusually  acute 
angle  designates  low  arterial  tension  and  a  free  peripheral  blood- 
flow,  while  a  blunt  or  rounded  apex  having  an  obtuse  angle  is  a  sign 
of  high  tension  and  obstruction  to  the  peripheral  circulation.  The 
former  accompanies  the  vigorous  systoles  and  relaxed  arterial  ten- 
sion of  Corrigan's  disease,  and  the  latter  is  commonly  due  to  arterio- 
sclerosis, aortic  stenosis,  and  aneurism.  It  is  important  also  to 
remember  that  a  blunt  apex  tracing  is  frequently  the  result  of  ex- 
cessive tension  of  the  sphygmograph  spring  or  of  a  misfit  between 
the  metal  pad  of  the  instrument  and  the  patient's  artery. 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       331 

The  Spacing,  Height,  and  Direction  of  the  Upstroke. — Regular 
spacing  of  the  upstrokes  means  rhythmic  beating  of  the  pulse,  the 
rate  of  which  may  be  determined  either  by  counting  the  strokes  of 
the  stilet  or  by  attaching  a  chronograph  to  the  sphygmograph. 
Arhythmia  is  shown  by  irregularity  in  the  length  of  the  upstroke 
intervals,  which  should  be  carefully  measured  with  a  pair  of  dividers 
in  order  to  fix  the  degree  and  the  type  of  the  arhythmia  in  the  case 
in  question.  A  spurious  form  of  arhythmia  may  be  produced  by 
some  fault  in  the  mechanism  that  drives  the  smoked  paper  slip, 
which  if  it  travels  too  fast,  imitates  the  closely  spaced  strokes  of  a 
rapid  pulse,  or  which,  if  it  moves  too  slowly,  simulates  the  wide 
spacing  of  a  slow  beat. 

The  height  of  the  upstroke  is  a  rough  index  of  the  pulse  volume, 
the  stroke  being  either  long  or  short  according  to  whether  the  volume 
be  ample  or  deficient.  A  perpendicular  upstroke,  the  apex  of  which 
is  very  high  above  the  base  line,  reflects  vigorous  contraction  of  the 
left  ventricle.  Decided  obliquity  of  the  upstroke  suggests  some 
impediment  to  the  normally  vigorous  impact  of  the  systolic  blood- 
column,  the  slow  distention  of  the  arteries  being  referable  to  such 
factors  as  weakness  of  the  left  ventricle,  high  arterial  tension,  aortic 
stenosis,  mitral  insufficiency,  or  aneurism.  In  studying  the  upstroke 
it  must  always  be  remembered  that  this  detail  of  the  sphygmogram 
varies  with  the  tension  of  the  wrist-band  and  the  spring  of  the  instru- 
ment, as  well  as  with  the  approximation,  exact  or  imperfect,  of  the 
metal  plate  to  the  patient's  artery. 

The  Strength  of  the  Downstroke  Waves. — A  diminutive  tidal  wave 
indicates  diminished  force  or  volume  of  the  arterial  blood-flow,  as, 
for  example,  in  simple  cardiac  asthenia,  in  undue  peripheral  relaxa- 
tion, and  in  regurgitant  defects  of  the  aortic  and  mitral  valves.  An 
exaggerated  tidal  wave,  on  the  other  hand,  suggests  high  arterial 
tension,  as  in  conditions  attended  by  fibrosis  and  atheroma  of  the 
arteries.  A  feeble  recoil  wave  occurs  in  high  arterial  tension,  and 
the  level  of  such  a  wave  is  abnormally  high  above  the  base  line; 
in  states  of  low  tension  this  wave  is  comparatively  well  marked. 
Numerous  oscillations  and  subsidiary  downstroke  waves  are  fre- 
quently observed  on  the  tracing  as  a  consequence  of  a  high-tension 
pulse. 

Changes  in  the  Arterial  Wall  and  Caliber. — The  diminished 
resiliency  of  a  sclerotic  arterial  wall  conveys  to  the  palpating  finger 
a  sense  of  increased  resistance  which  becomes  more  and  more  striking 
as  the  fibrosis  progresses,  until  finally  the  affected  vessel  is  converted 
into  a  rigid,  tortuous  tube,  either  more  or  less  symmetrically  thickened 
or  beaded  with  spots  of  local  calcification.  A  sclerotic  and  a  high- 


332  PHYSICAL   DIAGNOSIS 

tension  vessel  are  distinguishable  by  suppressing  the  pulse-beat 
with  the  proximal  and  distal  fingers,  while  the  mural  condition  is 
examined  with  the  middle  finger.  Since  peripheral  sclerosis  does 
not  necessarily  imply  similar  implication  of  the  deeper  arteries, 


Fig.  129. — Brachial  arteriosclerosis.     (Jefferson  Hospital.) 

such  -as  the  aorta  and  the  coronaries,  thickening  of  the  radials  alone 
does  not  warrant  a  diagnosis  of  general  arteriosclerosis,  to  detect 
which  all  the  accessible  arteries,  as  well  as  the  heart,  should  be 
examined. 

Changes  in  the  size  of  the  vessel,  due  to  increase  in  its  caliber,  are 
closely  related  to  the  volume  of  the  pulse,  to  be  referred  to  later, 
although  personal  peculiarities  also  account  for  variations  in  the 
size  of  the  arteries,  quite  apart  from  cardiovascular  influences. 

Disturbances  of  the  Pulse-rate. — Fundamentally,  deviations 
from  the  normal  pulse-rate  are  referable  to  defective  function  of  the 
controlling  nerves  of  the  heart  and  to  variations  in  arterial  tension. 
Thus,  the  pulse  beats  with  increased  frequency  if  the  sympathetic 
nerves  of  the  cardiac  ganglia  are  excited  by  stimulation,  if  the 
vagus  loses  its  restraining  influence  through  depression,  or  if  the 
vis  afronte  is  lessened  by  subnormal  arterial  tension.  On  the  con- 
trary, the  pulse-rate  is  slowed  by  depression  of  the  sympathetic  or 
of  the  ganglia,  by  stimulation  of  the  vagus,  and,  usually,  by  the 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       333 

increased  effort  of  the  heart  provoked  by  high  arterial  tension. 

Increase  of  the  pulse-rate,  giving  rise  to  the  pulsus  frequens,  is 
symptomatic  of  the  abnormally  rapid  cardiac  action  known  as 
tachycardia  (Fig.  130,  i).  Exceptionally  there  are  persons  who  can 
voluntarily  accelerate  the  pulse-rate,  perhaps  by  a  psychic  in- 
fluence upon  the  vagus  and  the  accelerator  nerves.  Increased  fre- 
quency of  the  pulse  attends,  with  a  certain  parallelism,  most 
febrile  states,  the  pulse  rising  about  eight  beats  above  normal  for 
each  degree  of  fever,  and  in  children  attaining  even  a  higher  ratio. 
To  this  general  rule  there  are  numerous  exceptions,  notably  yellow 
fever,  tuberculous  meningitis,  pneumonia,  and  enteric  fever,  in  all 
of  which  hyperpyrexia  and  a  relatively  slow  pulse  may  coexist.  The 
same  is  often  true  of  fevers  complicated  by  uncompensated  car- 
diovascular diseases.  On  the  other  hand,  the  pulse-rate  is  frequently 
found  to  be  disproportionately  high  to  the  pyrexia  in  sepsis,  phthisis, 
scarlatina,  and  acute  miliary  tuberculosis.  Nervous  disturbances 
commonly  account  for  a  rapid  pulse,  as  in  the  neurasthenias,  so-called 
irritable  heart,  nervous  palpitation,  paroxysmal  tachycardia,  and 
Graves'  disease.  Undue  frequency  of  the  pulse  is  also  a  familiar 
sign  in  locomotor  ataxia,  anterior  poliomyelitis,  acute  ascending 
paralysis,  cerebral  concussion,  vagus  neuritis  and  compression,  and 
sympathetic  irritation.  Pain,  whatever  its  cause,  generally  accounts 
for  tachycardia  of  more  or  less  degree.  Circulatory  defects,  due  to 
valvular  or  mural  lesions  of  the  heart,  to  pericarditis,  to  cardiac 
displacement,  and  to  the  state  of  collapse,  greatly  disturb  the  pulse- 
rate,  variously  exciting  increase  or  a  diminution,  as  well  as  interfering 
with  the  normal  rhythm.  One  looks  for  a  quick  pulse  after  hemor- 
rhage, after  aspiration  of  a  large  exudate,  in  the  essential  anemias, 
in  Addison's  disease,  and  in  arthritis  deformans.  Other  factors 
of  abnormal  pulse  rapidity  include  the  toxic  effects  of  belladonna 
and  aconite,  and,  in  most  persons,  the  immoderate  use  of  alcohol, 
tea,  coffee,  and  tobacco  acts  similarly,  though  in  others  just  the 
opposite  effect  may  be  produced. 

The  atropin  reaction,  or  an  increase  in  the  pulse-rate  by  the  ac- 
tion of  atropin  on  the  vagus,  is  sometimes  used  by  clinicians  as  a 
test  of  cardiac  competency.  If  the  integrity  of  the  heart  be  un- 
impaired, the  pulse-rate  increases  from  30  to  40  beats  per  minute 
within  one-half  hour  after  a  hypodermic  injection  of  from  -5^  to  ^5- 
grain  of  atropin,  but  in  a  subject  of  myocardial  degeneration  no  such 
acceleration  occurs.  This  test  is  used  by  Talley  in  cases  of  auricular 
fibrillation  (v.  i.)  to  determine  whether  vagal  tone  or  cardiac  muscle 
is  the  main  factor,  and  he  finds  in  such  cases  after  full  digitalization 
that  atropin,  after  a  preliminary  period  of  slowing  of  the  pulse, 


334 


PHYSICAL   DIAGNOSIS 


subsequently  accelerates  it  if  the  vagus  be  at  fault,  while  a  much 
less  marked  reaction  is  noted  if  the  cardiac  muscle  be  structurally 
diseased.  A  similar  release  of  the  vagal  action  has  been  observed 
in  the  slow  pulse  of  meningitis  (Roch  and  Cottin).  Amyl  nitrite, 
which  has  the  advantage  of  instantaneous  effect,  has  an  action 
similar  to  that  of  atropin,  and  can  be  used  as  its  substitute  under 
identical  conditions. 

In  judging  a  pulse-rate  the  accelerating  influence  of  mental 
unrest,  physical  exertion,  and  the  digestive  period  should  be  taken 
into  account.  It  is  not  without  interest  also  to  remember  that  a 
normal  pulse  perceptibly  quickens  as  the  result  of  violent  coughing, 
as  well  as  after  Valsava's  experiment  of  forced  expiration  with  the 
mouth  and  nose  closed. 

Auricular  tachycardia  is  met  with  in  auricular  flutter,  a  condi- 
tion in  which  the  normal  auricular  contractions  are  replaced  by 


Fig.  izga. — Electrocardiogram  of  auricular  flutter.   (Tracing  by  Dr.  E.  B.  Krumbhaar.) 

abnormal  impulses,  of  rapid  rate  and  perfect  rhythm,  springing 
from  auricular  foci  away  from  the  sino-auricular  node,  and  occur- 
ring at  a  rate  of  from  200  to  300  or  more  beats  per  minute.  So 
accelerated  are  these  new  systoles  of  the  auricles  that  true  dias- 
tole of  these  chambers  cannot  take  place,  and  ordinarily  but  a 
part  of  the  contractions  are  shared  by  the  ventricles,  for  many  of 
the  waves  are  blocked  by  the  bundle  of  His.  While  the  auricles 
beat  at  a  3oo-per-minute  rate,  the  ventricles  may  beat  but  one-half 
or  one-fourth  as  fast,  though  exceptionally  a  temporary  (and 
dangerous)  phase  develops  wherein  the  ventricular  pulse  equals 
the  auricular  rate.  Chronic  myocarditis,  arteriosclerosis,  and  a 
history  of  rheumatism,  syphilis,  or  gout  are  the  common  ante- 
cedents of  this  type  of  tachycardia,  which  is  commoner  in  the  aged 
than  in  the  young.  It  is  prone  to  persist  for  years,  and,  as  Lewis 
points  out,  "a  constant  repetition  of  the  same  high  pulse  at  inter- 
vals of  weeks  or  months"  strongly  suggests  the  presence  of  such 
a  lesion.  In  some  cases  the  rapid  auricular  beats  are  clearly  be- 
trayed by  jugular  pulsations  in  the  neck,  and  deep  pressure  in  the 
carotid  region,  so  as  to  irritate  the  vagus,  causes  an  appreciable 
slowing  and  intermission  of  the  arterial  pulse.  A  full  dose  of  digi- 
talis acts  similarly. 
On  the  sphygmogram  numerous  a-waves  of  regular  contour  and 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       335 

height  fill  the  diastolic  (Vf)  period  of  the  tracing,  and  the  arte- 
rial waves  vary  in  regularity  and  number,  depending  upon  the 
integrity  of  the  heart's  conduction  path.  The  electrocardiogram 
shows  a  multiplicity  of  small,  sharp  P-waves  of  undue  rapidity 


Fig.  1296. — Electrocardiogram  showing  leads  I,  II,  III  of  auricular  flutter  with  in- 
complete heart-block  and  extreme  tachycardia.  Note  uniformity,  definition,  and 
incidence  of  P-waves,  and  irregularity  and  variable  height  of  /?-waves.  Auricular  rate 
600,  and  ventricular  rate  200,  per  minute.  (Tracing  by  Dr.  E.  B.  Krumbhaar.) 

and  striking  regularity ;  or  the  oscillations  immediately  preceding 
the  ventricular  complex  may  be  so  rapid  and  delicate  as  to  form 
merely  a  blurred  streak  before  the  /?-waves  (Fig.  1290).  The  latter 
are  grouped  irregularly,  or  are  typical  of  an  orderly  incidence 
between  every  third  or  fourth  auricular  undulation,  according  to 
the  degree  of  existing  heart-block.  The  accompanying  electro- 
cardiogram (Fig.  1 296)  illustrates  the  irregularity  of  the  waves  in 
leads  I,  II,  III  in  a  case  of  auricular  flutter  with  delayed  and 
intermittent  conduction  of  the  impulses. 


336  .     PHYSICAL   DIAGNOSIS 

Paroxysmal  tachycardia  is  a  condition  which  arises  in  response 
to  new  and  abnormal  impulses  originating  in  foci  far  removed  from 
the  sino-auricular  node,  whose  action  is  overshadowed  by  that  of 
the  ectopic  stimuli  which  excite  a  pulse-rate  varying  from  100  to 
200  beats  per  minute,  in  paroxysms  lasting  from  a  few  seconds  to  as 
long  as  many  hours  or  even  days.  As  a  rule,  this  rapid  rate  is 
initiated  in  the  auricle,  less  commonly  in  the  ventricle,  but  in 
either  event  it  remains  rhythmic,  despite  variations  in  the  force 
of  the  individual  arterial  f pulse-beats.  The  paroxysms  of  tachy- 
cardia begin  most  abruptly  and  end  with  equal  suddenness,  and  but 
immaterial  acceleration  of  the  pulse  is  provoked  by  physical  exer- 
cise. Mental  and  physical  stress,  flatulence,  and  gastro-intestinal 
disorders  usher  in  most  attacks,  and  myocardial  degeneration, 
coronary  artery  sclerosis,  and  mitral  stenosis  are  familiar  findings 
in  those  cases  in  which  pathologic  defects  are  found. 

The  arterial  sphygmogram  clearly  indicates  the  onset  of  the 
paroxysm  by  a  line  of  exceedingly  rapid  and  small  waves  of  equal 
height,  often  preceded  by  a  few  premature  auricular  systoles. 
The  venous  tracing  shows  corresponding  rapidity,  and  may  be 
either  undisturbed  or  demonstrate  obliteration  of  the  t'-waves  by 
the  a-waves.  In  the  electrocardiogram  there  are  numerous  ven- 
tricular complexes  which  tend  to  encroach  upon  and  even  to  oblit- 
erate the  preceding  P-waves,  whose  increased  height  and  inversion 
are  sometimes  conspicuous. 

Diminution  of  the  ptilse-rate,  betrayed  by  the  pulsus  rarus,  signi- 
fies an  unduly  slow  cardiac  action  termed  bradycardia  (Fig.  130,  II). 
In  certain  individuals  this  condition  does  not  appear  to  be  un- 
natural (Napoleon's  pulse  averaged  but  40  beats  per  minute),  and 
a  pulse-rate  of  50  or  60  a  minute  may  exist  habitually  without 
being  of  itself  incompatible  with  perfect  health;  any  noteworthy 
diminution  below  these  figures,  particularly  if  it  persists,  calls  for 
inquiry  as  to  some  pathologic  factor.  In  studying  the  slow  pulse  it 
is  essential  to  determine  that  the  peripheral  pulsations  are  a  true 
index  of  the  contractions  of  the  heart:  impairment  of  the  cardiac 
power  may  be  of  such  a  character  that  only  the  alternate  ventric- 
ular systoles  are  strong  enough  to  produce  a  perceptible  radial 
pulse,  thus  creating  a  fictitious  pulsus  rarus.  An  inordinately  slow 
pulse  is  symptomatic  of  various  disorders  of  the  heart  and  blood- 
vessels, and  of  these  factors  it  is  well  to  remember  fibroid  and  fatty 
heart,  coronary  artery  sclerosis,  general  arterial  sclerosis,  aortic 
stenosis,  and  Stokes-Adams  disease.  Many  nervous  diseases  are 
commonly  attended  by  the  pulsus  rarus — meningitis,  cerebral  tumor 
and  hemorrhage,  depressed  fracture  of  the  skull,  lesions  of  the 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       337 

medulla  and  of  the  upper  cord,  epilepsy,  mania,  paresis,  and  myx- 
edema.  A  slow  pulse  is  generally  found  during  the  apneic  period 
of  Cheyne-Stokes  respiration,  in  the  postfebrile  stages  of  many 
acute  infections,  in  grave  cachexias,  in  the  toxemias  of  icterus, 
diabetes,  uremia,  ergotism  and  saturnism,  and  in  poisoning  by 
digitalis,  strophanthus,  convallaria,  conium,  and  opium.  Pain, 
which  generally  accelerates  the  pulse,  and  chronic  indigestion, 
which  acts  similarly,  may  under  certain  circumstances  consider- 
ably retard  its  frequency. 

The  combination  of  bradycardia,  diminished  pulse  volume,  and 
hypotension  constitutes  the  oculocardiac  reflex  of  Aschner,  a 
phenomenon  attributable  to  a  true  trigeminovagus  reflex  action. 
This  trilogy  of  signs,  notably  the  slowing  of  the  pulse  8  to  10  beats 
a  minute,  occurs  promptly  in  fully  70  per  cent,  of  healthy  subjects 
after  firm  compression  of  the  eyeball  with  the  pulp  of  the  finger. 
The  reaction  is  within  normal  limits  in  nervous  bradycardia,  in 
states  of  arterial  hypertension,  and  in  most  cases  of  paroxysmal 
tachycardia,  although  Lian  finds  that  it  is  sometimes  possible  to 
slow  the  heart  in  the  last-named  disorder  by  prolonged  bilateral 
ocular  pressure.  The  oculocardiac  reflex  is  lost,  as  a  rule,  in  tabes; 
and  it  is  conspicuous  in  Graves'  disease,  in  epilepsy,  in  gastro- 
intestinal neuroses,  and  in  various  toxemias,  notably  in  nicotin- 
poisoning.  An  "inverted"  reflex,  distinguished  by  an  acceleration 
of  the  pulse  after  ocular  compression,  has  been  observed  in  incipi- 
ent cases  of  exophthalmic  goiter  and  in  many  emotional  states. 

Irregularity  and  Intermission. — The  radial  pulsations,  which 
normally  take  place  at  regular  intervals  coincident  with  ventric- 
ular systole,  are  subject  to  various  disturbances  of  rhythm  con- 
sisting of  irregularities  and  intermissions,  conforming  in  certain 
instances  to  well-defined  types.  On  the  other  hand,  there  are  also 
pulse  irregularities  that  lack  definite  sequence  in  their  series  of 
beats,  and  in  which  the  tempo  is  much  disordered,  the  individual 
beats  being  separated  by  a  confusion  of  long  and  short  intervals. 
Pulse  irregularity  indicates  some  impairment,  either  functional  or 
structural,  of  the  cardiac  force,  whereby  its  contractions  deviate 
from  their  normal  periodicity  and  generally  also  fail  in  power, 
the  irregularities  of  time  being  attended  by  inequalities  in  the 
volume  and  power  of  the  separate  beats.  As  already  intimated 
in  a  preceding  paragraph,  an  intermittent  pulse  is  not  an  infallible 
sign  of  an  intermittent  heart,  since  the  systoles,  though  rhythmic, 
may  not  all  produce  an  appreciable  pulse  at  the  wrist.  The 
pulsus  intermittens,  a  general  term  for  intermissions  of  the  peri- 
pheral pulse,  must  always  be  distinguished,  by  auscultation  of  the 


338  PHYSICAL   DIAGNOSIS 

heart,  from  the  pidsus  deficiens,  in  which  the  intermission  depends 
upon  actual  failure  of  the  heart  to  contract.  An  allorrhythmic 
pulse  is  distinguished  by  rhythmic  irregularities,  or  those  in  which 
the  disordered  pulse  rhythm  is  definitely  systematic  and  periodic 
(pidsus  inequalis  periodicus).  To  this  type  belong  the  bigeminal 
pulse  (pulsus  bigeminus),  distinguished  by  two  beats  and  a  pause, 
and  the  trigeminal  pulse  (pidsus  trigeminus) ,  consisting  of  three  beats 
and  a  pause,  recurring  in  orderly  succession,  these  peculiar  allorrhyth- 
mias  being  most  commonly  found  in  mitral  disease,  especially  after  full 
doses  of  digitalis  or  one  of  its  cogeners  (Fig.  130,  rv,  v).  The  inter- 
ruption of  a  rhythmic  sequence  of  beats  by  a  minor  beat  distinguishes 
the  pulsus  intercidens.  In  the  alternating  pulse  (pidsus  alternans)  there 
is  a  series  of  strong  and  feeble  beats  alternating  in  regular  succession. 
This  type  of  pulse  is  most  often  found  in  the  aged,  and  is  a  grave 
sign,  in  that  it  indicates  a  progressive  exhaustion  of  the  cardiac 
muscle,  attending  lesions  such  as  arteriosclerosis,  myocardial 
fibrosis,  angina  pectoris,  and  chronic  nephritis.  The  use  of  the 
sphygmomanometer  in  clearly  identifying  the  alternating  pulse 
has  been  referred  to  elsewhere.  (See  p.  33.) 

The  paradoxic  pulse  of  Kussmaul  (pulsus  paradoxus),  character- 
ized by  bilateral  enfeeblement  or  disappearance  of  the  radial  pulse 
during  inspiration,  is  not  distinctive  of  any  special  condition,  though 
it  is  not  uncommonly  demonstrable  in  adhesive  pericarditis,  pericar- 
dial  effusion,  mediastinal  inflammation  and  tumor,  and  extreme 
cardiac  asthenia.  Sometimes  Kussmaul's  pulse  may  be  closely 
imitated  at  will  simply  by  holding  the  breath  after  having  taken  a 
deep  inspiration.  Inspiratory  disappearance  of  one  radial  pulse  has 
been  noted  in  adhesion  of  the  subclavian  artery  to  the  pleura. 

In  seeking  for  a  cause  of  an  irregular  pulse,  it  should  be  remem- 
bered that  this  peculiarity  may  be  of  no  consequence  whatever, 
especially  when  it  appears  temporarily.  It  is  frequently  traceable  to 
emotional  disturbances,  physical  strain,  neurasthenia,  indigestion, 
constipation,  and  the  misuse  of  tobacco,  tea,  and  coffee.  Old  people 
and  young  children  sometimes  have  a  persistently  irregular  pulse, 
with  nothing  tangible  to  account  for  it.  But  it  is  another  story 
when,  aside  from  these  influences,  the  subject's  arhythmia  is  con- 
stant and  associated  with  subjective  symptoms  and  with  signs  of 
cardiac  disturbance,  under  which  circumstances  one  naturally  in- 
vestigates first  the  cardiovascular  and  then  the  nervous  systems. 
These  sources  of  an  irregular  pulse  are  referred  to  under  Cardiac 
Arhythmia.  (See  p.  363.) 

Variations  in  the  Tension,  Volume,  and  Velocity  of  the  Pulse. 
— Tension. — The  tension  of  the  pulse-wave  is  regulated  by  the  force 


EXAMINATION   OF    THE    CARDIOVASCULAR   SYSTEM          339 

and  rate  of  the  ventricular  systole  and  the  volume  of  blood  thereby 
propelled,  by  the  degree  of  peripheral  resistance,  and  by  the  elasticity 
of  the  arteries.  Thus,  a  powerful,  rapid  heart  and  a  well-contracted 
set  of  peripheral  vessels  together  make  for  inordinately  high  tension — 
hypertension ;  while  a  feeble,  slow  heart  and  a  toneless,  relaxed 
vasomotor  system  give  subnormal  tension — hypotension.  In  most 
instances  these  factors  are  not  so  well  balanced  as  in  the  academic 
illustrations  just  drawn,  for,  owing  to  their  unequal  action,  the 
effects  of  certain  factors  tend  to  be  neutralized  by  the  influences  of 
others — normal  arterial  tension  may  be  preserved  even  in  collapse, 
should  the  hypotension  of  the  vasomotor  depression  be  negatived 
by  the  recuperative  overaction  of  the  heart.  Usage  establishes 
the  terms  pulsus  durus  and  pulsus  mollis,  the  former  designating  the 


Fig.  I2QC. — Electrocardiogram  of  a  case  of  arterial  hypertension,  showing  the  large 
r-wave  of  vigorous  ventricular  contraction.     (Tracing  by  Dr.  T.  A.  Cope.) 

tense,  hard,  non-compressible  pulse  of  hypertension,  and  the  latter 
denoting  the  relaxed,  soft,  readily  compressible  pulse  of  hypotension 
(Fig.  130,  VI,  VII).  Of  the  latter,  two  special  types  have  been 
described:  the  extraordinarily  soft  and  empty  gaseous  pulse,  and 
Motineret's  pulse,  soft,  slow,  full,  and  quite  distinctive  of  the  toxemia 
of  icterus. 

Clinically,  it  is  desirable  to  estimate  the  maximum  or  systolic, 
the  minimum  or  diastolic,  and  their  difference  or  the  pulse,  pressures, 
data  accurately  obtainable  only  by  using  a  sphygmomanometer.  (See 
p.  31.)  Only  roughly  is  it  possible  to  gage  arterial  tension  by 
ordinary  digital  examination,  though  some  general  idea,  later  to  be 
elaborated  instrumental^,  may  be  gained  by  compressing  the  radial 
artery  in  the  manner  described  above,  and  by  noting  both  the  force 
of  the  pulse  and  the  fulness  of  the  vessel  between  the  beats.  Thus, 
with  three  fingers  laid  upon  this  vessel,  the  degree  of  pressure  exerted 
by  the  proximal  finger  to  obliterate  the  pulse  approximates  the 


I.  Pulsus  frequens. 


II.  Pulsus  ranis. 


III.  Pulsus  inequalis. 


IV.  Pulsus  bigeminus. 


V.  Pulsus  trigeminus. 


VI.  Pulsus  durus. 


34° 


VII.  Pulsus  rnollis. 


VIII.  Pulsus  dicroticus. 


IX.  Pulsus  anacroticus. 


X.  Pulsus  bisferiens. 


XI.  Pulsus  magnus. 


XII.  Pulsus  parvus. 


XIII.  Pulsus  celer. 


XIV.  Pulsus  tardus. 

Fig.  130. — Sphygmograms  of  pathologic  types  of  the  arterial  pulse.     (Tracings  by 
Dr.  G.  Bachmann.) 

341 


342  PHYSICAL   DIAGNOSIS 

systolic  pressure,  provided  that  the  pulse  under  examination  is  not 
of  too  full  a  volume.  Using  the  same  technic,  the  diastolic  pressure 
is  suggested  by  estimating  the  force  necessary  to  bring  out  the 
greatest  impact  of  the  pulse-beats,  which,  as  the  pressure  of  the 
fingers  increases,  gradually  becomes  stronger  and  stronger,  attains 
an  acme,  and  then  diminishes.  It  is  also  worthy  of  note  that  a 
radial  artery  palpable  between  pulse-beats  suggests  hypertension, 
and  that  one  which  is  indistinguishable  indicates  hypotension,  the 
influence  of  fibrocalcareous  changes  being,  of  course,  excluded. 

In  a  pulse  of  low  tension  and  usually  of  full  volume  the  dicrotic 
or  recoil  wave  is  frequently  appreciable,  by  gentle  palpation,  as  a 
secondary  impact  immediately  following  the  principal  beat.  This 
exaggeration  of  the  normal  dicrotic  wave  (pulsus  dicroticus)  is  well 
shown  in  febrile  states  and  exhaustion  attended  by  extreme  arterio- 
capillary  dilatation,  in  uncompensated  mitral  regurgitation  which 
restricts  the  ventricular  output  of  blood,  and  in  posthemorrhagic 
anemia  severe  enough  to  diminish  the  volume  of  arterial  blood 
(Fig.  130,  VIII).  The  pulse  is  described  as  hyperdkrotic  when  the 
dicrotic  wave  of  the  sphygmogram  falls  below  the  base  of  the  sys- 
tolic upstroke,  and  a  pulse  of  this  sort  suggests  very  low  tension  and 
increased  cardiac  rate  and  force. 

Occasionally,  as  the  result  of  hypertension  and  tardy  filling  of 
the  aorta  (as  in  extreme  aortic  stenosis) ,  the  predicrotic  or  tidal  wave 
is  palpable  just  after  the  systolic  beat  (pulsus  bisferiens).  That 
this  predicrotic  impact  is  associated  with  high  tension  and  is  most 
distinctly  developed  by  firm  pressure  upon  the  artery  serves  to  dis- 
tinguish it  from  the  dicrotic  wave,  which  accompanies  low  tension 
and  is  detected  only  by  gentle  or  moderate  pressure.  A  tracing  of 
the  pulsus  bisferiens  shows  a  double  apex  composed  of  upstroke 
and  tidal  wave,  the  latter  sometimes  being  the  more  conspicuous 
(Fig.  130,  X). 

Another  variety  of  high-tension  pulse,  also  met  with  in  aortic 
stenosis,  is  characterized  by  a  notched  upstroke  or  anacrotic  limb, 
and  hence  is  known  as  the  pulsus  anacroticus  (Fig.  130,  IX).  The 
upstroke  interruption  of  this  type  of  pulse  means,  according  to 
Mackenzie,  "  that  the  lever  of  the  sphygmograph  has  been  raised 
in  the  first  instance  slightly  quicker  than  the  following  current  of 
blood,  and  as  the  distending  wave  increases,  the  returning  lever  is 
caught  and  carried  along  to  the  summit."  The  anacrotic  pulse, 
then,  reflects  augmented  contractile  power  at  the  end  of  systole,  and 
does  not  indicate  a  real  interruption  of  the  ventricular  contraction. 

In  general,   hypertension  accompanies  diffuse  arterial   sclerosis, 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM        343 

cardiac  hypertrophy,  angina  pectoris,  apoplexy,  uremia,  nephritis, 
and  adequately  compensated  aortic  regurgitation.  Hypotension  is 
to  be  expected  as  the  effect  of  shock  and  collapse,  extensive  frank 
or  concealed  hemorrhage,  acute  febrile  diseases,  exhausting  cachexias 
and  anemia,  primary  myocarditis,  cardiac  dilatation,  and  valvular 
lesions,  such  as  extreme  aortic  stenosis  and  mitral  leakage,  which 
diminish  the  ventricular  output  of  blood  with  systole. 

Volume. — The  volume  of  the  pulse,  or  the  extent  of  the  arterial 
expansion  produced  by  the  pulse-wave,  varies  with  the  size  of  the 
vessel's  caliber  and  with  the  volume  and  force  of  the  systolic  blood- 
column.  The  more  yielding  the  walls  of  the  artery  under  the  influ- 
ence of  the  systolic  blood- wave,  the  greater  the  volume  of  the  pulse, 
of  which  the  chief  determining  factors  are,  apart  from  the  size  and 
force  of  the  systolic  wave,  the  degree  of  intra-arterial  pressure  and 
the  inherent  tension  of  the  arterial  walls.  In  general  terms,  then, 
it  follows  that  with  an  equal  systolic  output  of  blood,  peripheral 
dilatation  and  hypotension  increase,  and  that  peripheral  constriction 
and  hypertension  diminish,  the  volume,  or  size,  or  amplitude  of  the 
pulse.  In  health,  aside  from  the  physiologic  exaggeration  during 
inspiration,  the  individual  pulse-beats  are  of  equal  volume  (pulsus 
equalis),  and,  unless  modified  by  anatomic  peculiarities,  there  is 
also  a  similar  bilateral  symmetry.  Inequalities  of  volume  (pulsus 
inequalis)  are  generally  associated  with  irregularities  of  rhythm  and 
rate,  the  causes  of  which  have  been  dealt  with  sufficiently  in  a  fore- 
going paragraph  (Fig.  130,  III). 

Increase  of  the  pulse  volume  (pulsus  magnus)  commonly  attends 
conditions  provocative  of  subnormal  arterial  tension,  and  is  recog- 
nized by  the  palpating  finger  as  an  unnatural  expansion  of  the 
vessel  at  the  time  of  the  pulse-beat  (Fig.  130,  XI).  Jerkily  arhyth- 
mic  pulsations  of  undue  volume  are  sometimes  spoken  of  as  the 
"caprizant"  or  "goat-leap"  pulse.  The  full,  bounding  pulse  of 
fevers,  the  large  pulse  of  cardiac  overaction  or  hypertrophy,  and  the 
momentarily  voluminous  pulse  of  aortic  valve  leakage  typify  the 
pulsus  magnus.  Overfulness  of  the  artery  during  the  interval 
between  pulsations  (pulsus  plenus)  indicates  a  large  volume  of  blood 
within  the  vessel,  irrespective  of  its  size — a  small,  tense,  contracted 
artery  may  be  just  as  full,  relatively,  as  one  which  is  large,  soft,  and 
relaxed. 

Diminution  of  the  pulse  volume  (pulsus  parvus)  is  attended  by  but 
slight  stretching  of  the  vessel-wall  during  the  beat,  and  is  not  infre- 
quently combined  with  arhythmia  and  with  increased  arterial  tension 
(Fig.  130,  XII).  A  small  pulse  may  depend  upon  deficient  cardiac 


344  PHYSICAL   DIAGNOSIS 

force,  or  upon  lesions  that  diminish  the  volume  of  blood  in  the  periph- 
eral vessels.  The  former  accounts  for  the  subnormal  pulse  volume  in 
collapse,  in  conditions  attended  by  malnutrition  and  exhaustion,  and 
in  the  various  functional  and  structural  weaknesses  of  the  heart;  the 
latter  explain  the  small  pulse  in  stenoses  of  the  aortic  and  mitral 
orifices,  in  aneurism,  and  in  certain  cases  of  profound  anemia,  the 
arterial  blood-column  being  obstructed  in  the  first  instance,  diverted 
in  the  second,  and  actually  reduced  in  bulk  in  the  last.  The  arach- 
noid pulse,  small,  thread-like,  and  running,  is  a  good  example  of  the 
excessive  diminution  of  pulse  volume  symptomatic  of  extreme 
circulatory  depression.  A  pulse  whose  volume  and  force  gradually 
taper  off  has  been  described  as  the  decurtate  or  mouse-tail  pulse. 
Emptiness  or  collapse  of  the  artery  between  beats  is  indicated  by 
diminished  amplitude  of  the  pulse  during  such  intervals  (pulsus 
vacuus),  and  is  dependent  upon  grave  cardiac  enfeeblement,  or 
inadequate  ventricular  filling  in  mitral  leakage,  or  an  unsustained 
arterial  blood-column  due  to  aortic  insufficiency. 

Velocity. — The  rapidity  with  which  the  individual  waves  rise  and 
fall  is  referred  to  as  the  velocity  or  celerity  of  the  pulse.  A  quick 
pulse  (pulsus  celer),  or  one  whose  undulations  are  abrupt,  gives 
rise  to  a  series  of  sharp  tapping  beats,  which,  irrespective  of  their 
volume,  quickly  recede  from  the  palpating  finger.  Subnormal  arte- 
rial tension  is  suggested  by  this  type  of  pulse,  the  steep,  high  strokes 
of  which  are  clearly  shown  by  the  sphygmographic  tracing  (Fig. 
130,  XIII).  The  trained  observer  has  little  difficulty  in  recognizing 
the  pulsus  celer  without  instrumental  aid,  if  care  be  taken  to  differ- 
entiate the  sharp  bounding  pulse  of  increased  volume:  the  two  may 
resemble  each  other  in  so  far  as  the  rise  of  the  wave  is  concerned,  but 
in  the  latter  the  pulse-wave,  though  sharp,  lacks  a  rapid  descent  and 
is  fairly  well  sustained.  The  pulsus  celer  may  be  symptomatic  of 
arteriocapillary  relaxation,  incident,  for  example,  to  fever,  collapse, 
debility,  and  anemia,  but  its  acme  is  attained  in  the  pulsus  celerrimus 
of  Corrigan's  disease,  in  which  left  ventricular  hypertrophy,  relaxed 
peripheral  vessels,  and  a  leaky  aortic  orifice  combine  to  create  a 
poorly  sustained  pulse-wave  of  extraordinary  velocity  and  volume. 
A  tardy  pulse  (pulsus  tardus)  rises  and  falls  slowly  and  is  well  sus- 
tained, independently  of  the  frequency  of  its  beats.  The  impact 
of  this  pulse,  which  is  to  be  expected  when  the  arterial  tension  is  high, 
conveys  to  the  palpating  finger  the  sensation  of  a  slowly  rising  wave 
of  rather  prolonged  duration  and  deliberate  fall,  which  peculiarities 
are  traced  by  the  sphygmograph  as  a  curve  of  moderate  amplitude, 
oblique  upstroke,  rounded  apex,  and  gently  declining  downstroke, 


EXAMINATION   OF    THE    CARDIOVASCULAR    SYSTEM       345 

marked  by  feeble  secondary  oscillations  (Fig.  130,  XIV).  Pure 
aortic  stenosis  is  the  factor  of  the  most  typical  examples  of  the 
pulsus  tardus,  owing  to  the  slow  ventricular  contractions  and  de- 
layed passage  of  the  blood-stream  through  the  narrow  aortic  orifice. 
Arteriosclerosis,  hindering  the  prompt  rise  and  fall  of  the  pulse- 
waves,  is  also  an  important  cause  of  this  type  of  pulse. 

Asymmetry  of  the  Pulses. — Conditions  that  impede  the  normal 
passage  of  arterial  blood-waves  from  the  left  ventricle  to  the  periphery 
disturb  the  bilateral  symmetry  of  the  pulse-rate  and  volume,  by 
retarding  and  diminishing  the  waves  beyond,  and  on  the  same  side  as, 
the  lesion,  which  in  the  extreme  instance  may  produce  so  decided  an 
obstruction  to  the  blood-current  as  practically  to  extinguish  the  pulse 
in  the  distal  arteries  of  the  surface.  Inequalities  of  the  pulses  from 
such  causes  must  be  carefully  distinguished  from  those  due  merely 
to  abnormal  distribution  of  the  vessel  or  vessels  under  examination; 
and  it  is  also  to  be  recalled  that  the  left  radial  pulse  is  generally 
stronger  in  right-handed  individuals  and  in  the  ambidextrous. 

Taking  as  criteria  the  radial  arteries,  delay  and  enfeeblement 
of  one  pulse  at  the  wrist  suggest  aneurism,  of  the  ascending  aortic 
arch  or  of  the  innominate  artery  if  the  right  pulse  be  modified,  and  of 
the  transverse  arch  (to  the  left  of  the  innominate's  origin)  or  of  the 
descending  portion  if  the  left  pulse  be  altered.  Aneurismal  dilata- 
tion of  the  subclavian,  axillary,  or  brachial  arteries  are  also  to  be 
regarded  as  a  possible,  though  rare,  cause  of  suppressed  peripheral 
pulsations  on  the  same  side,  and  a  like  asymmetry  is  referable  to 
arterial  obstruction  by  embolism  or  thrombosis,  as  well  as  to  the 
pressure  of  cicatrices,  faultily  knit  fractures,  tumors,  and  intrathoracic 
effusion  of  fluid  and  of  air.  Retardation  of  both  carotid  pulses  in 
comparison  with  the  apex-beat  is  found  in  aneurism  of  the  ascending 
aorta,  while  the  right  carotid  beats  later  than  the  heart  in  aneurism 
of  the  innominate  artery.  Suppression  of  both  femoral  pulses  may 
mean  either  aneurism  of  the  abdominal  aorta  or,  most  exceptionally, 
congenital  obliteration  of  this  vessel;  inequality  in  the  force  of  the 
femorals  suggests  obstruction,  as  by  thrombosis  or  tumor,  of  the  feebly 
beating  vessel;  and  delay  of  the  femoral  pulse,  compared  with  the 
radial,  suggests  aortic  aneurism  below  the  arch. 

The  Capillary  Pulse. — The  capillary  pulse  of  Quincke,  which 
indicates  transmission  of  the  individual  pulse-waves  to  the  capil- 
laries, is  recognized  as  a  systolic  flushing  and  diastolic  pallor  of 
some  peripheral  part,  such  as  beneath  the  finger-nail — hence  the 
expression,  pidsus  subungualis.  To  show  it  in  this  situation  the  nail 
should  be  blanched  by  slight  pressure  on  its  tip,  whereupon  systolic 


346  PHYSICAL   DIAGNOSIS 

reddening  of  the  pale  subungual  area  is  readily  perceptible.  The  same 
thing  can  be  seen  upon  the  mucous  membrane  of  the  lower  lip  when 
it  is  everted  and  pressed  upon  with  a  glass  slide,  and  along  a  line  of 
hyperemia  rubbed  upon  the  forehead  with  some  blunt  instrument, 
such  as  the  cap  of  a  fountain-pen.  If  the  ophthalmoscope  be  used, 
one  can  also  observe  a  capillary  pulsation  of  the  retinal  arteries. 

Ordinarily,  no  pulse  is  visible  in  the  capillaries,  through  which  the 
blood  trickles  in  a  waveless  stream,  but  under  circumstances  that 
increase  cardiac  force,  diminish  capillary  resistance,  and  retard  venous 
return  flow,  the  pulsations  of  the  heart  permeate  as  far  as  the  small 
arteries  of  the  periphery  and  distend  them  with  each  systole.  Essen- 
tially, the  capillary  pulse  is  the  product  of  the  pulsus  celer  and  is 
associated  with  conditions  of  subnormal  arterial  tension.  It  is  a 
valuable  sign  of  aortic  regurgitation,  though  it  is  not  constant  in  this 
lesion,  nor  pathognomonic,  since  a  capillary  pulse  is  demonstrable  in 
many  conditions  underlying  the  pulsus  celer,  i.  e.,  fever  and  anemia, 
and,  moreover,  it  is  occasionally  noted  in  a  presumably  healthy  person. 

The  Venous  Pulse. — Ordinarily,  the  auricular  contractions  driving 
the  blood-stream  into  the  ventricles  fail  to  create  any  appreciable 
backward  wave  within  the  venae  cavae  and  pulmonary  veins,  since 
at  this  period  of  the  cardiac  cycle  the  auricular  outlets  of  these  vessels 
are  so  tightly  contracted  that  a  reflux  cannot  take  place.  When, 
however,  the  veins  are  unduly  distended  and  their  cardiac  orifices 
correspondingly  dilated,  the  contractions  of  the  heart  propel  blood- 
waves  not  alone  forward  into  the  arteries,  but  also  backward  into 
the  great  venous  trunks,  the  superior  caval  impulses  being  propa- 
gated into  the  veins  of  the  neck,  especially  on  the  right  side,  which 
show  pulsatile  movements,  either  presystolic  or  systolic  in  time, 
according  to  the  mechanism  at  work,  as  will  be  explained  presently. 
Occasionally  the  backward  waves  are  blocked  by  the  valves  just 
distal  to  the  jugular  bulb,  and  in  this  event  a  "bulbous  pulse"  is 
observed  at  the  root  of  the  neck,  above  the  sternoclavicular  articula- 
tion. But  usually  these  valves  leak,  so  that  there  is  visible  pulsation 
of  the  jugular  veins,  more  prone  to  occur  in  the  internal  jugular  than 
in  the  external,  though  the  latter's  pulsations  are  more  readily  detected, 
owing  to  its  superficial  situation.  The  venous  pulse  thus  produced 
serves  as  a  definite  index  to  the  action  of  the  right  auricle  and 
ventricle. 

The  venous  pulse  should  be  studied  while  the  patient  is  in  recum- 
bency, with  the  object  of  ascertaining  its  precise  site,  extent,  and 
time  relation  to  the  events  of  the  cardiac  cycle.  Pulsation  of  the 
internal  jugular  vein  may  be  very  similar  to  that  of  the  carotid  artery, 
but  the  jugular  pulse-wave  rises  gradually  and  falls  very  suddenly, 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       347 

frequently  causing  momentary  recession  of  the  overlying  tissues  at  the 
site  of  the  pulsation,  while  the  carotid  wave  rises  abruptly  and  forcibly 
but  falls  slowly  and  deliberately,  and,  moreover,  is  attended  by 
unnatural  arterial  throbbing  remote  from  the  cervical  region.  A 
true  venous  pulsation  travels  upward  from  the  root  of  the  neck  and 
produces  distention  and  rhythmic  throbbing  of  the  vein,  after  it 
has  been  emptied  from  below  upward  by  the  finger,  but  if  the  pul- 
sation be  transmitted  from  the  carotid  artery,  pressure  over  the  vein 
distends  it  and  exaggerates  the  pulsation  above  the  point  of  constric- 


Fig.  131. — Sphygmogram  of  the  normal  venous  and  arterial  pulses.    (Tracing  by 
Dr.  G.  Bachmann.) 

tion  below  which  the  vessel  collapses  and  becomes  pulseless.  These 
visual  signs  of  the  venous  pulse,  though  suggestive,  should  be  con- 
firmed by  means  of  a  graphic  tracing,  in  order  to  fix  the  exact  time 
of  the  movements  with  relation  to  those  of  the  heart,  and  by  instru- 
mental aid  of  this  sort  it  is  possible  to  determine  these  essential 
details,  and  to  recognize  two  distinct  types  of  the  venous  pulse,  the 
auricular  and  the  ventricular,  which  differ  very  materially,  from  a 
diagnostic  and  prognostic  viewpoint. 

The  auricular  or  presystolic  venous  pulse  is  due  to  the  contraction 
of  the  right  auricle,  and  represents  a  physiologic  or  negative  type  of 
pulsation,  for  it  may  occur  in  the  healthy  subject  in  consequence  of 
temporary  venous  distention,  induced,  for  example,  by  prolonged 
holding  of  the  breath.  The  sphygmogram  of  this  type  of  pulse 
(Fig.  132)  is  distinguished  by  a  succession  of  inordinately  high 
auricular  waves  (a),  timed  well  in  advance  of  the  carotid  impulse, 
as  shown  by  the  lower  tracing,  made  simultaneously  with  that  of  the 
jugular  movements.  The  systolic  wave  (5),  following  the  closure  of 


348  PHYSICAL   DIAGNOSIS 

the  tricuspid  valve  (3-4)  is  of  comparatively  moderate  amplitude, 
and,  after  the  period  of  auricular  filling  (Af),  is  succeeded  by  a  single- 
peaked  ventricular  wave  (z1),  after  which  the  ventricular  filling  (Vf) 
commences,  completing  the  diastolic  phase.  Comparing  this  sphyg- 
mogram  with  that  of  the  ordinary  jugular  pulsations  (Fig.  131; 
cj.  Fig.  14),  it  is  apparent  that  the  chief  characteristics  of  the  auricu- 
lar venous  pulse  are  an  exaggerated  a-wave,  a  moderate  s-wave,  and 
a  v-wave  of  pyramidal  outline  rather  than  doubly  undulated.  Clin- 
ically, this  type  of  pulse  means  adequate  nutrition,  contractility,  and 
force  of  the  right  auricle. 


Fig.  132. — Sphygmogram  of  the  auricular  or  presystolic  type  of  venous  pulse.  (Tracing 
by  Dr.  G.  Bachmann.) 

The  ventricular  or  systolic  venous  pulse  is  produced  by  the  con- 
traction of  the  right  ventricle,  and  typifies  the  variety  of  pulsation 
sometimes  described  as  pathologic  or  positive.  It  may  indicate 
tricuspid  leakage,  whereby  with  each  ventricular  contraction  a 
reflux  blood-column  is  propelled  back  into  the  right  auricle  and 
thence  into  the  venous  tributaries  of  this  chamber;  or  it  may  be 
due  not  so  much  to  actual  tricuspid  leakage  as  to  instant  filling  of 
the  auricle,  because  of  excessive  intravenous  pressure.  The  appear- 
ance of  such  a  pulse  suggests  auricular  enfeeblement,  with  com- 
paratively well-sustained  ventricular  power,  which,  despite  the 
coexistence  of  dilatation  sufficient  primarily  to  set  up  tricuspid 
regurgitation,  is  still  strong  enough  to  drive  backward  a  forceful 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       349 

reflux  wave.  The  sphygmogram  of  the  ventricular  venous  pulse 
(Fig.  133)  shows  an  unnaturally  high  and  blunt  ventricular  wave 
(v)  synchronous  with  the  midphase  or  late  phase  of  systole,  as  indi- 
cated by  the  comparable  carotid  tracing.  Pari  passu  with  progres- 
sive enfeeblement  of  the  right  auricle,  this  fl-wave  becomes  more 
and  more  conspicuous,  encroaches  upon  the  gradually  diminishing 
curves  of  the  a-wave,  and  finally  replaces  them  completely.  Thus, 
a  prominent  ventricular  wave  indicates  not  only  tricuspid  leakage 
and  auricular  hypertension,  but  also  compensatory  hypertrophy 


Fig.  133. — Sphygmogram  of  the  ventricular  or  systolic  type  of  venous  pulse.   (Tracing 
by  Dr.  G.  Bachmann.) 

of  the  right  ventricle,  and,  therefore,  it  may  be  considered  a  good 
index  of  the  nutrition  and  the  pumping  power  of  the  ventricle. 
With  a  loss  of  this  efficiency,  the  v-wave  correspondingly  diminishes, 
and,  should  advanced  myocardial  degeneration  exist,  this  undulation 
does  not  appear  on  the  tracing. 

The  Penetrating  Venous  Pulse. — A  penetrating  or  centripetal  venous 
pulse  is  sometimes  demonstrable  in  the  small  veins  of  the  extremities 
under  conditions  that  allow  the  transmission  of  the  arterial  pulse 
to  the  venules.  This  type  of  pulse  occurs  most  frequently,  if  not 
solely,  in  connection  with  Quincke's  capillary  pulse,  of  which  it  is 
merely  an  exaggeration,  since  the  venous  pulse  depends  upon  a 
systolic  arterial  impact  of  sufficient  force  not  only  to  jog  the  blood- 
columns  within  the  capillaries,  but  also,  to  penetrate  the  diminutive 
veins  beyond  them.  Obviously,  the  penetrating  venous  pulse  is  a 
product  of  the  pulsus  celer,  and  hence  it  is  to  be  looked  for  chiefly 
as  a  sign  of  aortic  leakage,  and  also  in  states  of  extreme  vascular 
relaxation  (v.  s.~). 


350  PHYSICAL   DIAGNOSIS 

PERCUSSION 

The  beginner  will  be  likely  to  regard  cardiac  percussion  as  a 
somewhat  bewildering  procedure,  and  even  the  experienced  clinician 
cannot  always  rely  upon  its  findings  as  incontestable.  A  cultivated 
ear,  a  sensitive  pleximeter  finger,  and  the  strict  adherence  to  a  routine 
technic  are  essential  for  the  best  results,  however  experienced  the 
examiner  may  be.  Presupposing  these  preliminaries,  it  is  possible, 
by  percussion  of  the  precordial  region,  to  determine  the  situation, 
the  size,  and  the  shape  of  the  heart;  to  detect  the  presence  of  an 
effusion  within  the  pericardial  sac;  and  to  fix  the  position  of  the  left 
anterior  pulmonary  border. 

The  Areas  of  Cardiac  Flatness  and  Dulness. — Normally, 
two  precordial  regions,  affording  respectively  flatness  and  dulness, 
can  be  distinguished  by  careful  percussion  of  the  heart:  an  inner 
area  of  flatness,  over  that  part  of  the  heart  within  the  cardiac  in- 
cisura  of  the  left  lung  and  lying  directly  against  the  chest-wall, 
without  the  interposition  of  pulmonary  tissue;  and  an  outer  area  of 
dulness,  overlying  that  part  of  the  heart  separated  from  the  chest- 
wall  by  the  intervening  pulmonary  borders  (Fig.  134).  Of  these 
two  regions,  which  together  compose  the  total  precordial  area,  the 
inner  is  ordinarily  designated  as  the  area  of  absolute  or  superficial 
dulness,  and  the  outer  as  that  of  relative  or  deep  dulness,  than 
which  terms  the  words  flatness  and  dulness  seem  clearer  and  more 
definite  acoustically.  The  anatomic  relations  of  these  two  zones 
are  shown  by  Fig.  135. 

The  area  of  cardiac  flatness  is  a  triangular  space  overlying  the 
right  ventricle,  and  affording,  on  gentle  percussion,  flatness  or  abso- 
lute dulness,  with  decided  resistance  to  the  pleximeter  finger.  The 
right  border  (perpendicular)  of  this  triangle  follows  the  left  sternal 
border  from  the  fourth  to  the  sixth  costal  cartilage;  the  left  border 
(hypotenuse)  extends  from  the  fourth  left  chondrosternal  articulation 
to  the  junction  of  the  left  parasternal  line  and  the  upper  border  of 
the  sixth  rib  (about  £  inch,  or  1.25  cm.  within  the  apex);  and  the 
lower  border  (base)  runs  from  this  point  somewhat  obliquely  upward 
to  join  the  lowest  extremity  of  the  right  border,  at  the  sixth  chondro- 
sternal junction.  The  base  of  the  triangular  flatness,  inasmuch  as 
it  blends  with  hepatic  flatness,  cannot  be  mapped  out  by  ordinary 
finger  percussion.  The  principal  object  of  mapping  out  the  area 
of  cardiac  flatness  is  to  decide  if  the  left  lung  be  either  cirrhotic  or 
emphysematous,  since  pulmonary  retraction  extends,  and  pulmonary 
overdistention  restricts,  this  inner  cardiac  zone,  while  its  extent  is 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM       351 


not  necessarily  altered  by  changes  in  the  size,  position,  and  shape 
of  the  heart. 

The  area  of  cardiac  dulness,  surrounding  the  triangle  of  flatness, 
approximately  corresponds  to  the  anterior  aspect  of  the  heart,  being 
the  surface  outline  chiefly  of  the  right  ventricle,  and,  to  a  minor  extent, 
of  the  right  auricle  and  left  ventricle.  Over  this  area  strong  percus- 
sion affords  dulness  blended  with  pulmonary  resonance,  and  attended 
by  a  correspondingly  modified  sense  of  resistance.  From  the  cardiac 
base  line  (upper  border  of  third  rib)  the  outer  dulness  of  the  heart 


Cardiohepatic  angle  — ___. 

Hepatic  dulness 

Hepatic  flatness  _ •£ 


Cardiac  dulness 
—  Cardiac  flatness 


Fig.   134. — Percussion  areas  of  cardiac  flatness  and  dulness. 

extends  vertically  along  the  right  sternal  border1  to  the  sixth  costal 
cartilage,  whence  it  follows  the  lower  border  of  the  heart  to  the  apex, 
and  then  curves  upward,  with  an  external  convexity,  to  join  the  base 
line  at  the  left  sternal  border.  The  area  thus  mapped  out  extends 
roughly  -J  inch  (I.Q  cm.)  beyond  the  triangle  of  cardiac  flatness, 
except  at  the  lower  border,  where  both  have  the  same  limit;  it  is 
impracticable  to  try  to  delimit  the  upper  border  from  the  area  of 

1 "  In  many  cases  the  whole  extent  of  the  sternum  furnishes  such  a  loud 
tone  that  the  deep  cardiac  dulness  is  really  limited  by  the  left  sternal  border  " 
(Sahli). 


352 


PHYSICAL    DIAGNOSIS 


vascular  dulness.  The  junction  of  the  horizontal  limit  of  hepatic 
dulness  with  the  right  lateral  line  of  cardiac  dulness  forms  an  approxi- 
mate right  angle  of  resonance  in  the  fifth  right  intercostal  space, 
close  to  the  sternal  border — the  cardiohepatic  angle  of  Ebstein. 

Postural  influences  account  for  alterations  in  the  extent  of  the  lat- 
eral cardiac  borders,  the  right  border,  when  the  subject  changes 
from  recumbency  to  the  erect  posture,  shifting  outward  about 
half  an  inch  (1.25  cm.),  while  the  left  border  extends  similarly  for 
half  this  distance.  It  is  obvious  that  these  postural  differences, 
relating  to  the  normal  heart,  are  greatly  exaggerated  when  dealing 
with  an  enlarged  heart. 

The  area  of  vascular  dulness,  overlying  chiefly  the  aorta  and  the 
superior  cava,  extends  between  the  sternal  margins  from  the  cardiac 
base  line  to  the  lower  borders  of  the  first  costal  cartilages.  Nor- 
mally, this  area  affords,  on  moderately  strong  percussion,  impaired 
osteal  resonance  that  shades  off  almost  imperceptibly  as  Louis' 
angle  is  approached.  Extension  of  the  vascular  area,  especially 
upward  and  toward  the  right,  with  or  without  definite  flatness  over 


Dull 


Flat        Dull 


Fig-  135. — Transverse  section  of  the  thorax,  illustrating  the  anatomic  relations  of 
the  areas  of  cardiac  dulness  and  flatness. 

the  sternum,  is  one  of  the  earliest  and  most  valuable  signs  of 
aneurism  of  the  aortic  arch  and  of  extensive  dilatation  of  this  vessel. 
Methods  and  Technic. — With  the  patient  either  semirecumbent 
or  lying  flat  on  the  back,  the  examiner  percusses  from  frank  pul- 
monary resonance  toward  the  precordia,  carefully  noting  the  tonal 
modifications  and  changes  in  resistance  that  occur  when  the  outer 
and  inner  cardiac  zones  come  within  the  percussion  sphere.  For 
clinical  purposes  it  is  generally  sufficient  to  outline  the  upper  level 
of  the  heart  at  the  left  of  the  sternum,  and  to  mark  its  two  lateral 
limits  on  either  side  of  this  bone.  This  is  usually  done  by  ordinary 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       353 

finger  percussion,  though  auscultatory  percussion  perhaps  gives 
more  dependable  results  and  sometimes  enables  one  to  determine 
the  upper  (cardiovascular)  and  the  lower  (cardiohepatic)  levels. 
Advocates  of  instrumental  percussion  claim  that  with  an  ivory  or 
a  vulcanite  pleximeter  all  the  cardiac  boundaries  can  be  accurately 
mapped  out. 

In  outlining  cardiac  dulness  percussion  is  carried  downward  from 
the  left  infraclavicular  region  along  the  sternal  and  parasternal 
lines,  to  fix  the  upper  border;  horizontally  inward  from  the  left  axilla 
along  the  third,  fourth,  and  fifth  interspaces,  to  designate  the  left 
border;  and,  finally,  from  a  resonant  point  in  the  right  mammary 
region  inward  along  the  third,  fourth,  and  fifth  interspaces,  to  indi- 
cate the  right  border.  The  points  along  these  percussion  lines  corre- 
sponding to  the  dulling  of  pulmonary  resonance  are  then  joined  by 
a  continuous  line,  to  represent  the  total  outer  dulness  of  the  heart, 
the  upper  sternal  base  line  and  the  lower  border  being  connected 
arbitrarily. 

In  mapping  out  the  area  of  cardiac  flatness  the  percussion  strokes 
are  directed  from  above  downward  midway  between  the  sternal  and 
parasternal  lines;  inward  on  the  right  side,  at  the  levels  of  the  fourth 
and  fifth  costal  cartilages;  and  inward  on  the  left  side  along  the 
fourth  and  fifth  interspaces.  Proceeding  in  this  manner,  the  per- 
cussion sound  successively  affords  resonance,  dulness,  and  flatness 
as  the  lungs,  the  lung-covered  heart,  and  the  exposed  heart  are 
traversed,  in  the  order  given. 

The  foregoing  technic,  which  meets  all  ordinary  demands,  will  reveal 
any  undue  extension  of  the  lateral  and  lower  left  borders  of  the  heart, 
indicative  of  this  organ's  enlargement.  The  accurate  delimitation 
of  the  outline  of  a  normal-sized  heart  is  next  to  a  physical  impossi- 
bility— aside  from  the  "personal  equation,"  the  continual  move- 
ments of  the  heart  and  the  depth  of  its  outer  margin,  the  individual 
differences  in  the  thickness  of  the  pulmonary  borders,  and  the  sonor- 
ous vibrations  of  the  sternum  make  the  attempt  futile,  in  so  far  as 
the  exact  correspondence  of  the  percussion  outline  to  fixed  anatomic 
landmarks  is  concerned.  The  same  comment  applies  to  percussion 
of  the  vascular  area,  the  extension  of  which  is  betrayed  chiefly  by 
unnatural  parasternal  dulness.  The  diagram  on  the  opposite  page 
(Fig.  135)  shows  the  anatomic  difficulties  that  beset  precise  delimita- 
tion of  the  cardiovascular  regions. 

Increased  Cardiac  Dulness. — Extension  of  the  area  of  cardiac 
dulness  depends  upon  both  intrinsic  and  extrinsic  factors,  the  former 
relating  to  changes  in  the  heart  itself  and  in  the  pericardium,  and 
23 


354  PHYSICAL   DIAGNOSIS 

the  latter  to  traction  and  pressure  exerted  upon  the  heart  by  adjacent 
structures. 

A  general  increase  in  the  area  of  cardiac  dulness,  particularly  of 
the  transverse  diameter,  is  encountered  in  bilateral  ventricular  hyper- 
trophy and  dilatation,  and  a  similar  change  is  sometimes  noted  in 
moderate-sized  pericardial  effusion.  Increased  flatness,  forming 
a  roughly  pyramidal  or  pear-shaped  figure,  is  symptomatic  of  an 
extensive  effusion  into  the  pericardium;  the  apex  of  such  a  flat  pyra- 
mid points  upward,  perhaps  as  high  as  the  second  interspace;  the 
borders  are  sharply  defined  from  the  surrounding  lung  resonance; 
the  boundaries  usually  extend  laterally  when  the  patient  leans  forward; 
and  the  cardiac  apex  is  partly  or  completely  obliterated.  Extension 
of  the  normal  area  of  the  heart,  without  actual  enlargement,  may 
be  due  to  cirrhotic  shrinkage  of  the  left  lung,  or  to  a  neoplasm  or 
an  aneurism  crowding  the  heart  forward  against  the  chest-wall. 

Increase  of  cardiac  dulness  to  the  right  is  suggestive  of  hypertrophy 
and  dilatation  of  the  right  heart,  less  commonly  of  moderate  peri- 
cardial effusion,  or  of  a  greatly  distended  inferior  vena  cava.  Such 
conditions  dull  the  normal  pulmonary  resonance  of  Ebstein's  cardio- 
hepatic  angle  in  the  fifth  right  interspace  at  the  sternal  edge. 

Increase  of  cardiac  dulness  to  the  left  and  downward  is  character- 
istic of  left  ventricular  hypertrophy  and  dilatation,  a  lesion  which 
also  displaces  the  apex-beat  in  the  same  direction,  and  modifies 
its  force  according  to  the  nature  of  the  predominant  myocardial 
condition. 

Decreased  Cardiac  Dulness. — Atrophy  of  the  heart  accounts 
for  a  corresponding  contraction  of  the  surface  boundaries  of  the 
organ,  and  in  that  rare  lesion,  pneumopericardium,  the  area  of  cardiac 
flatness  is  replaced  by  the  tympany  of  the  air-distended  pericardial 
sac.  In  phthisis  it  is  common  to  find  the  size  of  the  heart  smaller 
than  normal,  and  Adler  has  described  a  form  of  congenital  micro- 
cardia  in  hypochondriacal  subjects.  More  commonly,  how- 
ever, diminution  of  the  area  of  flatness  is  referable  to  some  extra- 
cardiac  cause — emphysema,  which  envelops  the  heart  with  a  hyper- 
resonant  covering  of  overdistended  lung ;  pleural  adhesions,  whereby 
a  resonant  pulmonary  border  may  be  permanently  anchored  di- 
rectly in  front  of  the  heart;  left-sided  pneumothorax,  whose  clear 
tympany  encroaches  upon  the  triangle  of  cardiac  flatness  and  per- 
haps displaces  it  toward  the  right.  Simple  gaseous  distention  of 
the  stomach  diminishes  the  flatness  of  the  heart  frota  below  upward 
and,  as  W.  Gordon  has  pointed  out,  gastric  cancer  reduces  or  even 
obliterates  the  cardiac  flatness,  in  the  recumbent  position. 

Recent  *-ray  studies  have  shown  that  the  size  of  the  normal 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       355 

heart  diminishes  after  muscular  exercise,  and  is  not  increased  by  a 
state  of  temporary  dilatation,  as  formerly  believed.  This  fact  has 
been  proved  conclusively  by  the  researches  of  Nicolai,  Zuntz,  and 
numerous  other  investigators,  who  corroborate  the  pioneer  work 
of  Moritz  on  this  subject.  Of  100  subjects  examined  teleront- 
genographically  by  Williamson,  the  vast  majority  of  normal  hearts 
responded  to  any  exercise  within  their  power  by  definite  contrac- 
tion, and  even  in  pathologic  hearts  the  same  tendency  was  noted 
in  one-half  of  the  cases  examined. 

Displacement  of  the  cardiac  area  is  determined  by  the  position  of 
the  heart's  impulse,  rather  than  by  percussing  out  the  dislocated 
area,  and  the  circumstances  under  which  the  various  cardiac  dis- 
placements occur  have  been  referred  to  at  length  under  the  Apex- 
beat.  (See  p.  317.) 

AUSCULTATION 

By  auscultation  of  the  precordial  area  one  judges  the  intensity, 
quality,  and  rhythm  of  the  cardiac  tones,  and  determines  the  presence 
or  absence  of  unnatural  adventitious  sounds  of  endocardial  and 
pericardial  origin.  Like  other  methods  of  examination,  auscultation 
of  the  heart  must  be  carried  out  systematically,  in  order  to  afford 
the  best  results,  the  four  different  valve  areas  being  studied  in  regular 
order  so  as  to  compare  and  correlate  the  various  sounds.  Thus, 
the  mitral  sounds  are  first  investigated,  and  then  the  aortic,  to  ascer- 
tain the  auscultatory  findings  relating  to  the  left  ventricle;  while  the 
sounds  afforded  by  the  tricuspid  and  the  pulmonic  valves  are  the 
key  to  similar  signs  pertaining  to  the  right  ventricle. 

The  heart-sounds  should  be  auscultated  with  the  patient  in  both 
the  recumbent  and  the  upright  position,  for  posture  has  a  decided 
modifying  effect  on  certain  heart-sounds,  notably  on  endocardial 
murmurs,  some  of  which  can  be  made  to  appear  and  to  vanish, 
virtually  at  will,  by  changing  the  subject's  posture.  (Cf.  p.  316.) 

The  advantages  of  the  binaural  and  the  monaural  stethoscope 
in  cardiac  auscultation,  and  the  application  thereto  of  the  trans- 
manual  method  of  auscultation  have  been  pointed  out  elsewhere. 
(See  p.  28.)  Abrahams  suggests  the  use  of  stethoscopic  auscul- 
tation of  the  voice  sounds  outside  the  upper  and  lateral  cardiac 
boundaries  as  a  substitute  for  percussion  in  delimiting  these 
lines.  The  examiner,  having  placed  the  stethoscope  in  the  .niter- 
spaces  over  the  pulmonary  tissue  several  inches  outside  the  con- 
ventional cardiac  limits,  auscultates  while  the  subject  repeats 
"ninety-nine"  in  a  low  voice,  and,  moving  the  bell  of  the  instru- 
ment toward  the  heart,  marks  the  several  points  at  which  the 


356  PHYSICAL   DIAGNOSIS 

pulmonary  fremitus  becomes  inaudible  and  the  sounds  become 
extrastethoscopic.  These  points  of  lost  vibration,  which  mark 
the  transition  from  sound-conducting  lung  to  non-conducting 
heart,  are  joined  later  with  a  line  to  represent  the  outer  boundaries 
of  the  entire  cardiac  area  (v.  s.). 

Auscultatory  or  Valve  Areas. — Four  different  auscultatory 
areas,  corresponding  to  the  puncta  maxima  of  the  separate  valvu- 
lar sounds,  are  made  use  of  in  cardiac  auscultation:  the  mitral, 
the  tricuspid,  the  aortic,  and  the  pulmonic  (Fig.  136).  These  areas 

— ,-,     represent  the  points  upon  the 

•fP^tik  precordia  at  which  the  sounds 

of  the  corresponding  valves 
are  most  distinctly  audible, 
and  they  do  not  overlie  the 
anatomic  seats  of  the  valves, 
all  of  which  lie  in  the  imme- 
diate neighborhood  of  the 
third  left  chondrosternal  artic- 
ulation. (See  p.  310.) 

The  mitral  area  is  indi- 
cated by  a  circle  about  i  inch 
(2.5  cm.)  in  diameter,  centered 
at  the  cardiac  apex,  or  at 
that  point  where  the  apical 
thrust  of  the  heart  impinges 
against  the  chest-wall  during 
systole. 

The  tricuspid  area  overlies 
{••••••••••B^Bfl       the  lower  end  and  right  half 

Fig.  136.— Auscultatory  areas  of  the  cardiac      of  the  Sternum,  from  the  fourth 

to  the  sixth  or  seventh  costal 

cartilages,  in  which  situation  the  right  ventricle  and  the  parietes 
are  in  close  relation. 

The  aortic  area  is  situated  at  the  sternal  end  of  the  second  right 
intercostal  space  and  costal  cartilage  (aortic  cartilage),  where  the 
aorta  and  the  aortic  valve  approach  nearest  to  the  surface  of  the 
chest. 

The  pulmonic  area  is  at  the  sternal  end  of  the  second  left  inter- 
costal space,  over  the  most  superficial  projection  of  the  pulmonary 
artery  and  valve. 

The  Normal  Cardiac  Sounds. — Each  beat  of  the  heart  is  accom- 
panied by  two  sounds,  audible  in  the  precordial  area  as  tones  having 
a  distinctive  grade  of  intensity  and  a  sui  generis  quality.  These 


EXAMINATION    OF   THE    CARDIOVASCULAR   SYSTEM       357 

tones,  which  occur  rhythmically  and  bear  a  definite  relation  to  the 
events  of  the  cardiac  cycle,  may  be  represented  by  the  monosyllables 
lup-dup?  The  //?/>-element  is  the  first  sound  of  the  heart,  and  is 
synchronous  with  ventricular  systole,  through  about  two-thirds  of 
which  phase  it  persists,  ending  in  a  gradual  diminuendo.  The 
dffp-element,  following  the  first  sound  after  a  brief  interval,  is  the 
second  sound  of  the  heart,  and  coincides  with  the  closure  of  the 
semilunar  valves  and  the  beginning  of  ventricular  diastole;  it  is 
relatively  short,  sharp,  and  of  abrupt  termination,  and  is  separated 
from  the  succeeding  /#/>-sound  by  a  comparatively  long  interval  of 
silence  (Fig.  137).  Phonetically,  the  rhythmic  succession  of  the 


Fig.  137. — The  normal  cardiac  sounds. 

two  sounds  may  be  sketched:  liip-dfip — lup-dftp — liip-dfip,  the 
interval  between  the  two  sound  elements  representing  the  short 
pause,  and  that  between  their  recurrence  the  long  pause,  of  the 
cardiac  cycle.  The  diagram  on  page  312  shows  the  relation  between 
the  normal  sounds  of  the  heart  and  its  cyclic  phases. 

The  first  sound,  synchronous  with  the  cardiac  impulse  and  relatively 
more  intense  at  the  apex  than  at  the  base  of  the  heart,  is  a  musculo- 
valvular  tone,  due  partly  to  the  muscular  rumble  of  the  contracting 
ventricles,  and  partly  to  the  sudden  vibratory  tension  of  the  mitral 
and  tricuspid  valves  at  the  time  of  their  closure.  The  first  factor 
accounts  for  the  dull,  prolonged,  booming  quality  of  the  sound 
(muscular  tone),  and  the  second  explains  its  tinge  of  high-pitched 
sharpness  (valvular  tone).  Under  normal  conditions  the  character 
of  the  first  sound  is  subject  to  individual  variations,  being,  for  exam- 
ple, shorter,  higher  pitched,  and  more  valvular  in  slim,  spare  sub- 
jects than  in  those  whose  covering  of  muscle  and  fat  is  abundant. 

The  mitral  first  sound  is  more  prolonged  and  a  trifle  lower  in 
pitch  than  the  tricuspid — a  difference  that  can  be  detected  by  careful 
auscultation  of  the  separate  ventricular  elements  of  the  sound  at  the 

JWith  tolerable  constancy  it  is  also  possible  to  distinguish,  in  perfectly 
healthy  persons,  a  third  cardiac  sound,  audible  at  the  apex  as  a  faint  tone 
directly  after  the  dup  of  the  second  sound,  or  during  the  beginning  of  the  dias- 
tolic  period.  Thayer  suggests  that  this  so-called  "  third  heart-sound "  may 
be  caused  by  sudden  tension  of  the  mitral  and  possibly  the  tricuspid  valve  oc- 
curring during  the  protodiastolic  phase.  The  sound,  which  is  especially  clear 
in  the  young,  is  sometimes  accompanied  by  a  synchronous  impulse  which  may 
be  both  visible  and  palpable,  is  intensified'by  left  lateral  recumbency  and  dur- 
ing expiration,  and  is  commonest  in  subjects  with  a  slow  pulse. 


PHYSICAL   DIAGNOSIS 

mitral  and  the  tricuspid  areas.  This  difference  is  especially  notic- 
able  in  early  life;  it  is  to  be  explained  possibly  by  assuming  an  intrin- 
sically louder  mitral  sound,  certainly  by  the  fact  that  the  lung  between 
the  apex  of  the  left  ventricle  is  too  thin  to  affect  the  sound-waves 
arising  within  this  chamber,  while  over  the  right  ventricle  it  is  thick 
enough  to  dampen  the  sound  therein  produced. 

The  second  sound,  caused  by  the  closure  of  the  aortic  and  pul- 
monic  semilunar  valves,  totally  lacks  muscular  tone,  and  is  of  a 
purely  valvular  character;  normally,  it  is  louder  at  the  base  than  at 
the  apex.  In  the  young  the  pulmonic  second  sound  is  louder 
and  higher  pitched  than  the  aortic;  in  middle  life  the  intensity  of 
the  two  sounds  does  not  differ  materially;  and  in  advanced  age  the 
aortic  element  is  the  more  striking.  The  gradual  increase  in  the 
intensity  of  the  aortic  second  sound  is  doubtless  to  be  referred  to  the 
progressive  rise  in  the  aortic  blood-pressure  incident  to  maturity  and 
to  old  age.  Normally,  the  aortic  tension  is  higher  than  the  pulmo- 
nary, but  this  physiologic  factor  of  a  relatively  louder  aortic  second 
sound  is  offset  by  the  deep  situation  of  the  aorta  and  its  valve,  in 
contrast  to  the  superficial  position  of  the  pulmonary  artery  and  its 
valve. 

In  the  majority  of  healthy  subjects  of  all  ages  the  cardiac 
sounds  above  the  ensiform  cartilage  have  a  peculiar  superficial 
scratching  or  crunching  quality  intensified  by  forward  inclination 
of  the  trunk  and  by  lateral  decubitus.  This  sound,  called  "xiphis- 
ternal  crunching"  by  M.  Solis-Cohen,  has  a  resemblance  to  peri- 
cardial  friction,  but  it  is  regarded  as  a  purely  physiologic  sign, 
referable  perhaps  to  tensional  changes  in  the  loose  areolar  tissue 
of  the  sternopericardial  ligament  acted  upon  by  the  movements 
of  the  heart,  as  suggested  by  Bloomer. 

Changes  in  the  Intensity  and  Quality  of  the  Cardiac  Sounds. — 
The  normal  intensity,  tone,  and  quality  of  the  heart-sounds  are 
variously  modified  in  consequence  of  numerous  factors  intrinsically 
active  or  related  to  parts  acoustically  intimate  with  the  heart.  In 
attempting  to  judge  these  variations,  due  allowance  is  to  be  made  for 
the  influence  upon  the  normal  sounds  of  the  muscular  and  adipose 
development  of  the  subject — the  thin-chested  and  cadaverous  have 
relatively  louder  heart-sounds  than  the  muscular  and  obese,  or  than 
the  woman  with  generous  breasts. 

The  intensity  of  both  sounds  is  markedly  increased  in  cardiac 
hypertrophy,  since  in  this  condition  of  overdevelopment  both  the 
muscular  and  the  valvular  components  of  the  heart-tones  are  greatly 
exaggerated  (Fig.  138).  To  a  lesser  degree  the  sounds  are  magni- 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       359 

fied  by  simple  cardiac  overstimulation,  due,  for  example,  to  transient 
mental  excitement  or  to  the  effect  of  alcohol,  coffee,  and  like  stimu- 
lants; or  the  change  may  be  incident  to  one  of  the  cardiac  neuroses, 
to  Graves'  disease,  and  to  the  effects  of  an  incipient  febrile  affection. 
Pulmonary  consolidations  are  capable  of  conducting  the  cardiac 


Fig.  138. — Accentuation  of  both  cardiac  sounds. 

sounds  with  abnormal  intensity,  while  pulmonary  fibrosis  with 
shrinkage  may  expose  the  precordia,  and  thus  make  the  sounds  more 
superficial  and  apparently  louder  to  the  examiner's  ear.  Surgical 
emphysema  of  the  tissues  in  front  of  the  heart  may  greatly  amplify 
the  cardiac  tones  (Keats) . 

Intensified  cardiac  sounds  with  conspicuous  alteration  of  their 
quality  are  audible  when  neighboring  structures  are  so  changed  as 
to  act  as  a  resonating  chamber  for  the  normal  tones.  Thus,  it  is 
possible  for  the  heart-sounds  to  be  echoed  as  a  loud,  metallic,  hollow 
ring  by  a  distended  stomach  or  gut,  by  a  large,  empty,  clean-cut 
phthisical  cavity,  and  by  a  pneumothorax. 


Fig.   139.— Enfeeblement  of  both  cardiac  sounds. 

Both  sounds  of  the  heart  are  enfeebled  and  muffled  in  myocarditis, 
in  dilatation,  and  in  the  cardiac  asthenia  attending  conditions  of 
collapse,  shock,  paralysis,  and  great  debility  (Fig.  139).  Pleural  and 
pericardial  effusions  and  hypertrophic  emphysema,  by  covering  the 
apex,  also  lessen  the  normal  vigor  of  the  sounds.  In  that  rare  clinical 
curiosity,  pneumopericardium,  the  sounds  are  usually  far  away 
and  faint;  rarely  they  are  louder  than  normal,  amphoric,  and  bell- 
like.  In  high-grade  anemic  states  it  is  common  to  hear  sharp  slap- 
ping cardiac  sounds,  which,  though  perhaps  louder  than  in  health, 
are,  nevertheless,  to  be  interpreted  as  irritably  weak. 

Accentuation  of  the  First  Sound  at  the  Apex  (Fig.  140). — That 
the  first  sound  at  the  apex  is  likely  to  be  exaggerated  by  nervous 
excitement,  by  physical  exertion,  and  by  flatulence  should  always 
be  recalled  in  examining  a  patient  for  the  first  time.  The  turbulent 
character  of  this  sound  in  the  high-strung  neurotic  person  or  in  the 


36° 


PHYSICAL   DIAGNOSIS 


dyspeptic  is  not,  per  se,  to  be  construed  as  an  evidence  of  disease. 
In  ventricular  hypertrophy,  particularly  of  the  left  side,  the  first  sound 
resembles  a  sustained,  booming  rumble,  which,  though  often  muffled 
and  impure,  gives  one  the  impression  of  being  more  intense  than 
normal.  In  dilatation  of  this  cavity  the  first  sound  is  short,  sharp, 


140. — Accentuation  of  the  first  cardiac  sound. 


and  high  pitched,  being  not  unlike  the  valvular  tone  of  the  second 
sound.  A  loud,  high-pitched,  snappy  first  sound  at  the  apex  is  an 
important  diagnostic  sign  of  mitral  stenosis.  In  incipient  myo- 
carditis, in  the  early  stages  of  the  acute  febrile  diseases,  and 
throughout  the  whole  course  of  the  febriculae,  the  apical  first  sound 
is  commonly  more  or  less  accentuated  and  sharp. 


Fig.   141. — Enfeeblement  of  the  first  cardiac  sound. 

Enfeeblement  of  the  First  Sound  at  the  Apex  (Fig.  141). — Diminished 
intensity  of  the  apical  first  sound  betrays  weakness  of  the  ventricles, 
which  in  some  instances  is  so  marked  that  the  sound  is  practically 
inaudible.  Shock,  great  anemia,  collapse,  vagus  paresis,  extreme 
cardiac  dilatation,  and  myocardial  degeneration  (as  in  the  typhoid 
state  and  in  various  forms  of  myocarditis)  are  factors  by  which  the 
normal  strength  of  this  sound  is  modified.  In  mitral  regurgitation 
the  first  sound  is  enfeebled,  but  this  is  difficult  to  detect  because  of 
the  associated  systolic  murmur  which  partly  or  wholly  masks  the  ven- 
tricular tone  at  the  apex. 


Fig.   142. — Accentuation  of  the  second  cardiac  sound. 

Accentuation  of  the  Second  Sound  at  the  Base  (Fig.  142).  The 
character  of  the  aortic  and  pulmonic  second  sounds  at  the  base  of 
the  heart  is  of  the  greatest  clinical  value,  since  the  former  reflects 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM        361 

the  strength  of  the  left  ventricle  and  the  latter  the  vigor  of  .the  right 
ventricle.  In  judging  the  relative  intensity  of  the  two  sounds  their 
physiologic  differences  must  always  be  considered  in  the  light  of  a 
modifying  element.  Accentuation  of  the  aortic  second  sound,  the 
correlative  of  an  intensified  mitral  first  sound,  is  a  sign  of  increased 
arterial  tension  within  the  aorta  and  the  systemic  circulation.  This 
may  arise  from  purely  normal  causes,  such  as  temporary  vasomotor 
stimulation,  a  simple  overacting  heart,  and  pregnancy.  Or  the 
loudness  and  ringing  quality  of  the  sound  may  depend  upon  arterial 
sclerosis,  aortitis,  nephritis,  and  atheroma,  dilatation,  or  aneurism 
of  the  aorta.  In  hypertrophy  of  the  left  ventricle  with  competent 
aortic  valve  segments  a  similar  accentuation  is  also  audible.  Accen- 
tuation of  the  pulmonic  second  sound,  the  basic  equivalent  of  an 
intensified  tricuspid  first  sound,  develops  in  consequence  of  heightened 
pressure  within  the  pulmonary  circulation;  it  is. excited  by  lesions 
that  impede  the  blood-stream  within  the  lesser  circuit,  as  typical 
examples  of  which  may  be  named  pneumonia,  and  congestion,  emphy- 
sema, and  cirrhosis  of  the  lungs.  In  hypertrophy  of  the  right  ven- 
tricle the  pulmonic  second  sound  rings  loudly  so  long  as  the  intra- 
ventricular  pressure  is  not  high  enough  to  produce  a  "safety-valve" 
tricuspid  leakage  (q.  v.). 

Enfeeblement  of  the  Second  Sound  at  the  Base  (Fig.  143). — A 
weak,  indistinct  aortic  second  sound  commonly  results  from  myo- 
cardial  degenerations  of  varying  degrees  of  intensity,  and  from  general 


Fig.  14.3. — Enfeeblement  of  the  second  cardiac  sound. 

vasomotor  relaxation,  whereby  the  systemic  blood-pressure  is  lowered; 
it  may  also  be  due  to  profound  anemia,  as  in  the  posthemorrhagic 
form,  involving  a  transient  but  real  oligemia.  In  both  obstructive 
and  regurgitant  valvular  lesions  of  the  left  heart  this  sound  is  prone 
to  become  weak,  if  not  inaudible:  in  mitral  stenosis  and  in  mitral 
regurgitation,  because  the  tension  within  the  aorta  is  too  low  to  slam 
shut  the  aortic  valve  with  normal  force;  in  aortic  stenosis,  in  con- 
sequence of  the  deliberate,  noiseless  closure  of  the  sclerotic  and 
stiff  leaflets;  and  in  aortic  regurgitation,  owing  to  the  extensive 
valvular  deformity  and  to  the  bruit  of  the  diastolic  murmur.  Pul- 
monary lesions  that  impede  the  return  of  blood  to  the  left  side  ot 
the  heart  also  account  for  a  feeble  second  sound  at  the  aortic  car- 
tilage. 


362  PHYSICAL   DIAGNOSIS 

Weakening  of  the  pidmonic  second  sound  is  not  a  common  physical 
sign,  for  the  pressure  within  the  lesser  circulation  is  not  so  readily 
lowered  as  it  is  in  the  systemic  circuit.  Enfeeblement  of  this  sound 
invariably  supervenes  when  the  right  ventricle  weakens  and  dilates, 
and  it  is,  therefore,  a  distinctive  and  dependable  index  of  this  grave 
accident.  Tricuspid  regurgitation,  when  associated  with  right  ven- 
tricular weakness,  is  the  factor  of  a  feeble  second  sound  in  the 
pulmonic  area. 

Reduplication  of  the  Cardiac  Sounds. — Reduplication  or 
doubling  of  the  first  or  the  second  sound  of  the  heart,  less  commonly 
of  both  sounds,  is  heard  under  a  number  of  circumstances  whose 
direct  bearing  upon  these  phenomena  is  not  always  clear.  Three  dis- 
tinct sounds  in  each  cardiac  cycle  are  audible  when  a  single  (first  or 
second)  cardiac  tone  is  reduplicated;  four  sounds,  when  the  doubling 
affects  both  tones.  If  the  first  sound  be  reduplicated,  the  precordial 
sounds  may  be  imitated  thus:  lurrup-dup — liirrup-dfip;  if  the  second 
sound  be  doubled,  the  effect  will  resemble:  liip-durrup — lup-durrup. 
Single  reduplication  is  much  more  common  than  double,  and  splitting 
of  the  second  sound  more  frequent  than  of  the  first. 

In  certain  instances  the  reduplication  simulates  the  hoof-beats  of 
a  galloping  horse,  and  hence  is  termed  variously  bruit  de  galop,  or 
gallop  rhythm,  or  canter  rhythm;  in  other  cases  it  sounds  not  unlike 
the  double  beat  of  a  snare  drum — bruit  de  rappel.  In  the  former, 
the  doubled  elements  are  divided  by  a  brief  pause;  in  the  latter,  they 
occur  almost,  though  not  quite,  synchronously. 

Reduplication  of  the  first  sound  is  almost  invariably  heard  only 
at  or  near  the  apex,  being  audible  at  the  base  of  the  heart  only  as  a 
rare  exception  (Fig.  144).  It  is  not  a  true  reduplication,  but  rather 


Fig.  144. — Reduplication  of  the  first  cardiac  sound. 

an  apparent  doubling,  the  mechanism  of  which  is  probably  not  always 
identical.  Asynchronism  in  the  closure  of  the  mitral  and  tricuspid 
valves,  the  presence  of  an  obscure  presystolic  murmur,  unduly 
strong  auricular  action,  and  vibration  of  the  aortic  wall  are  four 
possible  causes  of  the  doubling.1  Systolic  reduplication  may  be 
met  with  in  mitral  disease,  in  arterial  sclerosis,  in  hypertrophy  and 

1  For  the  many  theories  of  systolic  doubling  the  reader  should  consult  the 
writings  of  Gibson,  Barr,  Sansom,  Bramwell,  Johnson,  Hayden,  Offenbacher, 
and  Guttman. 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM        363 

structural  degenerations  of  the  heart,  and  in  chronic  adhesive 
pericarditis. 

Reduplication  of  the  second  sound  is  most  commonly  heard  at  the 
base,  but  also  at  the  apex,  and  at  base  and  apex  coincidentally 
(Fig.  145).  Doubling  at  the  base  is  commonly  ascribed  to  asyn- 
chronous closure  of  the  semilunar  leaflets,  caused  by  unequal  tension 
in  the  general  and  the  pulmonary  circulations.  Owing  to  this  loss 
of  balance,  systole  of  the  ventricle  that  must  overcome  the  highest 
tension  is  delayed,  and  its  semilunar  valve  closure  is  correspondingly 
tardy.  This  type  of  doubling  may  occur  physiologically,  from 
forced,  full  inspiration;  it  is  pathologic  when  resulting  from  lesions 
upsetting  the  equilibrium  of  the  pulmonary  or  the  systemic  circuits. 
Therefore,  it  may  be  symptomatic  of  obstructive  lesions  of  the  lungs, 
arterial  sclerosis,  left-sided  valvular  defects,  myocarditis,  hyper- 
trophy, dilatation,  and  pericardial  effusion.  Reduplication  of  the 
second  sound,  heard  at  the  apex,  but  not  at  the  base,  is  apparent, 
rather  than  actual,  and  has  a  very  different  significance  from  the 
doubling  just  mentioned.  It  is  an  early  and  characteristic  sign  of 
mitral  stenosis,  and  almost  constantly  develops  in  advance  of  the 
presystolic  rumble  of  this  lesion.  The  forcible  entrance  of  the 
auricular  blood-column  produces  a  sudden,  sharp  tension  of  the 
mitral  curtains,  and  this  impact,  occurring  just  after  the  second 
sound,  counterfeits  a  doubling  of  the  latter. 


Fig.  145. — Reduplication  of  the  second  cardiac  sound. 

Arhythmia. — Disturbances  of  the  normal  rhythm  of  the  heart- 
beat may  depend  upon  structural  damage  to  the  cardiac  musculature, 
whereby  its  orderly  contractions  are  interfered  with,  or  they  may  be 
referable  to  erratic  action  of  the  vagus  and  sympathetic  nerves.  The 
former  factor  rules  in  the  arhythmia  attending  acute  infectious 
processes,  valvular  disease,  acute  cardiac  dilatation,  chronic  myocar- 
ditis, and  fatty  heart,  while  nervous  influences  are  particularly  active 
in  the  disordered  rhythm  incident  to  neuroses,  great  emotion,  intra- 
cranial  lesions,  gastro-intestinal  disturbances,  certain  toxemias,  and 
the  action  of  drugs  like  digitalis,  aconite,  and  belladonna. 

Simple  arhythmia  of  the  heart's  action  is  distinguished  by  various 
deviations  from  normal  force  and  rhythm,  and  a  heart  thus  affected 
may  afford  a  medley  of  intense  and  feeble  sounds  so  unequally  spaced 


364  PHYSICAL    DIAGNOSIS 

and  so  diverse  in  other  details  as  to  defy  comparison  and  description. 
Cardiac  arhythmia  reaches  a  climax  in  that  condition  of  extreme 
irregularity  and  palpitation  so  aptly  termed  delirium  cordis,  not 
infrequently  met  with  in  advanced  valvular  and  myocardial  disease. 
Disordered  cardiac  contractility  may  Account  for  the  presence  of 
alternately  loud  and  feeble  heart-sounds,  the  tactile  equivalent  of 
this  type  of  arhythmia  being  a  radial  pulse  whose  beats  are  alter- 
nately strong  and  weak — the  pulsus  alternans  (q.  r.).  Rhythmic 
irregularity  of  the  heart  is  designated  as  allorrhythmia. 

Intermittence,  or  the  omission  of  a  beat,  may  be  independent  of 
simple  irregularity,  but  the  two  are  commonly  associated.  Genuine 
intermission,  due  to  the  actual  omission  of  a  ventricular  systole,  is 
to  be  distinguished  from  simulated  intermission,  wherein  the  con- 
tractions of  the  ventricle  occur,  though  too  feebly  to  produce  a 
peripheral  pulse.  (Cj.  p.  336.) 

Respiratory  arhythmia  is  characterized  by  a  periodic  accelera- 
tion of  the  cardiac  rate  during  inspiration  and  a  slowing  of  the  rate 
during  expiration,  and  is  a  genuine  example  of  "sinus  arhythmia" 
depending  upon  alterations  in  the  tone  of  the  vagus.  In  young 
children  such  an  irregularity  is  peculiarly  common  with  ordinary 
respiratory  movements,  and  hence  has  been  designated  by  Mack- 
enzie as  the  "youthful  type  of  arhythmia";  in  adolescents  and  in 
young  adults  it  may  be  provoked  by  forced,  deep  respiration. 
Clinically,  respiratory  arhythmias  are  recognized  by  their  restric- 
tion to  early  life,  their  direct  relationship  to  respiratory  move- 
ments, and  the  perfect  correspondence  of  the  peripheral  pulse, 
the  precordial  impulse,  and  the  cardiac  sounds.  Sinus  arhyth- 
mias of  this  kind  are  not  of  serious  import,  and  are  promptly 
abolished  by  the  administration  of  atropin  and  by  other  factors 
of  rapid  cardiac  action,  such  as  pyrexia  and  muscular  exercise. 
They  show,  on  the  sphygmogram,  virtually  no  variation  of  the 
height  of  the  arterial  peaks,  and  on  the  electrocardiogram  no 
disturbance  of  sequential  contractions — merely  irregular  inci- 
dence of  the  beats. 

Extrasystolic  Arhythmia. — Extrasystoles,  or  premature  contrac- 
tions of  the  ventricles  and  the  auricles,  occur  in  consequence  of 
isolated  stimuli  arising  abruptly  in  parts  of  the  cardiac  musculature 
away  from  the  specialized  tissue  of  the  sino-auricular  node,  where 
the  normal  contraction  waves  begin.  Thus,  with  an  increased 
irritability  of  the  myocardium  as  a  factor,  numerous  ectopic  con- 
tractions are  suddenly  excited  prematurely  in  relation  to  the 
normal  systoles,  and  in  consequence  disturb  the. orderly  sinus 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       365 

impulses  of  the  heart.  This  type  of  arhythmia  is  commonest  in 
men  of  advanced  age,  and  in  those  who  show  evidences  of  myo- 
cardial  degeneration  and  of  valvular  lesions;  in  many  cases  there  is 
a  past  history  of  rheumatism,  in  others  it  is  associated  with  a  tem- 
perament of  nervous  unrest,  or  it  may  accompany  apparently  per- 
fect health.  The  use  of  tobacco  in  excess,  prolonged  and  fatiguing 
exercise,  arterial  hyper  tension,  and  digestive  disorders  are  additional 


Fig.   146. — Sphygmocardiogram  illustrating  extrasystolic  arhythmia.     Asterisks  indi- 
cate extrasystoles.     (Tracings  by  Dr.  G.  Bachmann.) 

provocative  causes  of  premature  contractions,  which  ordinarily 
subside  as  the  result  of  fever,  deliberate  apnea,  recumbency,  and 
moderate  muscular  exertion. 

The  occurrence  of  ventricular  extrasystoles,  wherefrom  irregu- 
larity, inequality,  and  intermission  of  the  heart's  contractions 
arise,  is  an  exceedingly  common  factor  of  disordered  rhythm 
(Fig.  146).  According  to  the  law  of  maximal  contraction  (Marie; 
Bowditch)  the  heart,  when  stimulated  to  contract,  does  so  with 


366  PHYSICAL   DIAGNOSIS 

its  maximal  power,  regardless  of  the  strength  of  the  stimulus. 
Furthermore,  each  contraction  thus  excited  completely  exhausts 
for  the  moment  the  energizing  material  of  the  cardiac  tissues 
essential  for  this  act,  and  until  this  material  again  accumu- 
lates in  sufficient  quantity,  fresh  stimuli  fail  to  excite  a  systole. 
Normally,  this  phase  of  cardiac  excitability,  termed  the  refractory 
period,  begins  just  before  the  time  of  systole  and  persists  throughout 
this  period,  the  heart  acquiring  more  and  more  sensitiveness  as 
diastole  progresses.  Abbreviation  of  the  refractory  period  and 
premature  stimulation  of  a  contraction,  whether  of  physiologic  or 
pathologic  origin,  result  in  an  extrasystole  timed  soon  after  the  normal 
beat.  Should  the  extrasystolic  refractory  period  overlap  the  time 
of  the  next  physiologic  stimulation,  the  ventricle,  being  at  this  time 
unresponsive,  cannot  react  to  the  stumulus,  and,  in  consequence, 
does  not  contract;  intermission  of  a  heart-beat  therefore  occurs. 
Extrasystolic  arhythmia  may  also  conform  to  a  regularly  intermittent 
type,  or  allorrhythmia,  the  superadded  contractions  occurring  in 
groups  of  two  or  of  three  successive  beats  followed  by  a  pause, 
and  producing  respectively  the  bigeminal  and  the  rrigeminal  pulse. 
This  variety  of  arhythmia  is  illustrated  by  the  sphygmograms  IV 
and  V  shown  on  page  340. 

Auricular  extr asystoles  are  regarded  as  contractions  excited  by 
abnormal  stimuli  arising  in  the  structure  of  the  auricles,  which, 
fatigued  by  these  aberrant  efforts,  fail  to  respond  to  the  immediately 
succeeding  normal  stimuli  originating  at  the  venous  mouths. 
Each  extrasystole  of  the  auricle,  therefore,  is  followed  by  a  long 
pause,  indicating  quiescence  of  both  auricles  and  ventricles,  and 
this  in  turn  is  followed  by  the  next  normal  contraction.  Both  the 
auricular  and  the  ventricular  types  of  extrasystole  affect  the  cardiac 
sounds  and  the  arterial  sphygmograms  similarly,  but  the  jugular 
tracing  of  the  auricular  type  clearly  shows  the  premature  auricular 
undulation,  followed  by  a  ventricular  wave  ushering  in  a  period  of 
passivity  before  the  next  normal  contraction  wave. 

Auriculoventricular  extr  asystoles,  in  which  the  premature  con- 
tractions are  of  nodal  origin,  are  characterized  by  synchronous  or 
almost  synchronous  contractions  of  the  auricles  and  ventricles, 
and  account  for  the  irregularity  known  as  nodal  or  a-v  rhythm. 
Inasmuch  as  the  contraction  impulse  is  displaced  from  its  normal 
situation  at  the  sino-auricular  node  to  a  site  in  the  junctional 
tissue  (the  a-v  node),  the  normal  a-v  interval  is  disturbed,  being 
either  greatly  abbreviated  or  indeed  quite  effaced,  so  that  the 
excitatory  waves  reach  the  auricles  and  ventricles  at  the  same  in- 


EXAMINATION    OF   THE    CARDIOVASCULAR    SYSTEM       367 

stant  and  thus  excite  synchronous  contraction  of  all  four  cardiac 
chambers;  if  the  ventricles  contract  before  the  auricles,  the  v-a 
interval  is  disturbed.  To  account  for  this  type  of  arhythmia  it  is 
assumed  that  the  secondary  nodal  center  initiates  contraction 
either  because  of  an  abnormally  slow  sinus  rhythm  or  that  it  does 
so  because  its  inherent  activity  is  disproportionately  enhanced. 
While  presenting  no  definite  subjective  symptoms,  the  jugular 
tracing  registers  an  abbreviated  a-s  interval,  a  blending  of  the  a-s 
waves  so  as  to  produce  a  bifurcated  systolic  peak,  or  an  appre- 
ciable reversal  of  the  a-s  undulations.  In  the  electrocardiogram 
inversion  of  the  P-wave  in  leads  II  and  III  is  the  rule,  owing  to 
the  change  in  the  direction  of  the  contraction  impulse,  and  in  some 
tracings  it  is  superimposed  upon  the  ventricular  undulations  R, 
S,  T,  which  otherwise  are  unaltered. 

Heart-block  Arhythmia. — Defective  conductivity  of  the  auriculo- 
ventricular  muscular  bundle  produces  a  type  of  irregularity  charac- 
terized by  dissociation  of  the  auricular  and  ventricular  rhythms, 


Fig.  1460. — Electrocardiogram  of  heart-block.     (Tracing  by  Dr.  T.  A.  Cope.) 

occurring  in  three  fairly  distinct  types:  incomplete  heart-block, 
complete  heart-block,  and  Stokes-Adams'  bradycardia. 

In  health  the  auricular  systole  takes  place  one-fifth  of  a  second  in 
advance  of  the  ventricular,  so  that  an  increase  in  the  tune-interval 
between  the  auricular  and  ventricular  contractions  argues  disturbed 
conductivity  of  His'  bundle,  the  function  of  which  is  the  conduction 
of  the  auricular  contraction  waves  to  the  ventricles.  When  this 
muscular  bridge  is  diseased  (as  by  syphilis,  fibrosis,  or  neoplasm) 
its  conductile  powers  are  crippled  and  a  corresponding  degree  of 
dissociation  of  the  auriculoventricular  systoles  is  produced.  Whip- 
ham  describes  a  congenital  form  of  heart-block,  ascribed  to  develop- 
mental defects  of  the  auriculoventricular  bundle. 

But  the  presence  of  pathologic  alterations  of  the  foregoing  nature 


368  PHYSICAL   DIAGNOSIS 

does  not  invariably  produce  heart-block,  for  the  cardiac  conducting 
paths  may  be  grossly  implicated  by  disease  without  any  conse- 
quent incoordination  of  the  auriculoventricular  contractions,  in 
which  group  of  cases  the  origin  of  the  impulses  in  Kent's  newly 
described  node  and  their  transmission  along  its  connecting  path- 
way are  to  be  assumed  (see  p.  313).  On  the  other  hand,  clinical 
heart-block  may  occur  without  pathologic  changes  in  the  bundle 
of  His,  the  sino-auricular  node,  or  Tawara's  node,  and  the  dis- 
ordered rhythm  in  instances  of  this  sort  is  usually  referred  to  pro- 
found vagal  depression. 

The  electrocardiogram  of  heart-block  (Fig.  1460)  shows  clearly 
the  dissociation  of  the  auricular  and  ventricular  beats,  as  demon- 
strated by  the  prolonged  P-R  intervals,  the  occasional  intermission 
of  the  R-T  waves,  and  the  regular  response  of  the  ventricular 
peaks  to  every  second  or  third  auricular  wave. 

Incomplete  heart-block  is  said  to  exist  when  some,  but  not  all,  of  the 
auricular  waves  fail  to  reach  the  ventricles,  which  in  consequence 
may  occasionally  miss  a  beat  at  irregular  intervals,  or  may  beat 
only  with  each  second,  third,  or  fourth  systole  of  the  auricles — a 
2:1,  3:1,  or  4:1  auriculoventricular  rhythm,  as  the  case  may  be. 

Complete  heart-block,  or  complete  obstruction  to  the  passage  of 
the  auricular  waves,  results  in  absolute  dissociation  of  the  auric- 
ular and  ventricular  systoles,  which  occur,  each  having  a  perfect 
rhythm  of  its  own,  independently  of  each  other. 

Stokes-Adams'  bradycardia  is  a  syndrome  characterized  by  slow 
ventricular  and  rapid  auricular  rates  of  contraction,  attended  by 
syncope,  epileptiform  convulsions,  and  visible  venous  pulsations 
in  the  neck,  which  ordinarily  occur  twice  or  thrice  oftener  than 
the  arterial  pulse-beats. 

Although  first  described  by  Thomas  Spens,  in  1 793,  this  symptom- 
complex  was  not  generally  accredited  as  a  clinical  entity  until 
half  a  century  later,  when  Stokes'  cases,  in  1842,  with  the  earlier 
work  of  Adams,  in  1827,  invested  it  with  the  eponym  by  which  it  is 
now  known.  Stokes-Adams'  disease,  which  may  occur  at  any  age, 
is  commonest  in  the  male  sex,  and  is  attributable  to  infections  such 
as  syphilis,  rheumatic  fever,  pneumonia,  diphtheria,  influenza, 
enteric  fever,  and  to  fatal  anaphylaxis.  Temporary  examples  of 
complete  heart-block  are  also  met  with  in  uremia,  and  incomplete 
block  is  readily  produced  by  overdigitalization  of  a  rheumatic 
heart.  The  pathologic  lesions  affecting  the  specialized  conducting 
tissues  of  His'  bundle  include  gumma,  neoplasm,  atrophy,  fibrosis, 
fatty  degeneration,  ulceration,  and  calcification;  and  the  damage 


EXAMINATION   OF    THE    CARDIOVASCULAR    SYSTEM       369 

to  the  heart  in  general  consists  of  inflammatory  changes  in  the 
cardiac  muscle  and  its  outer  and  inner  investments,  with  or  without 
sclerosis  of  the  coronary  arteries. 

Fibrillation  Arhythmia. — This  type  of  gross  irregularity  depends 
upon  fibrillation  of  the  auricles,  and  in  the  heart  so  affected  a  medley 
of  new  stimuli  arising  at  many  different  auricular  foci  replace  the 
fundamental  sinus  rhythm,  and  produce  a  persistent  disorder  of 
cardiac  rate.  During  these  confused  movements  of  the  auricle 
this  chamber  remains  stationary  as  a  whole  in  wide  diastole,  but 
its  muscular  fibers  throughout  are  extremely  active  and  the  wall 
"appears  to  be  alive  with  movement,  and  rapid,  minute,  and  con- 
stant twitchings  and  undulatory  movements  are  observed  in  a 
multitude  of  small  areas  upon  its  surface"  (Lewis).  The  ven- 
tricular contractions  are  wholly  incoordinate  with  the  auricular 
turmoil,  since  the  regular  succession  of  sinus  impulses  are  mingled 


Fig.  1466. — Electrocardiogram  of  auricular  fibrillation.    (Tracing  by  Dr.  T.  A.  Cope.) 

with  a  confusion  of  stimuli  which  escape  from  the  quivering  muscle- 
fibers  of  the  small  chambers.  According  to  the  conducting  proper- 
ties of  the  a-v  bundle,  the  rate  and  the  rhythm  of  the  ventricular 
contractions  vary  within  wide  limits  and  the  arterial  pulse  is  greatly 
disordered.  Commonly,  the  ventricular  contractions  number 
from  zoo  to  140  per  minute,  or  they  may  fall  to  as  low  as  40  or 
rise  to  as  high  as  200.  Originally  described  by  Mackenzie  as  a 
"nodal  rhythm,"  fibrillation  of  the  auricles  is  now  known  to  repre- 
sent the  birth  of  independent  contraction  stimuli  in  the  auricular 
wall  away  from  the  sino-auricular  node.  This  form  of  arhythmia 
is  found  in  fully  one-half  of  all  cases  of  mitral  stenosis,  and  in  many 
cases  of  advanced  myocarditis  and  arterial  sclerosis;  in  the  ex- 
ceptional case  alteration  hi  the  sino-auricular  node  (inflammation, 
fibrosis,  arteriosclerosis)  is  the  underlying  pathologic  cause. 
Clinically,  it  underlies  the  pulsus  irregularis  perpetuus  (q.  v.). 
24 


370  PHYSICAL   DIAGNOSIS 

A  peculiarity  found  in  most  cases  of  auricular  fibrillation  is  the 
wide  variation  of  the  maximal  and  minimal  systolic  blood-pressure 
figures — a  range  of  from  30  to  60  mm.,  in  Silberberg's  experience. 

In  the  electrocardiogram  (Fig.  1466)  the  auricular  P-wave  is 
replaced  by  a  series  of  very  fine  undulations,  signifying  the  auricu- 
lar fibrillations,  while  the  Q-R-S  waves  are  irregularly  spaced  and 
of  variable  height,  denoting  disordered  rate  and  force,  respectively. 

Ventricular  fibrillation,  with  gross  disorder  and  incoordinate 
contractions  of  the  musculature,  also  has  been  met  with,  as  the 
immediate  precursor  of  death,  in  light  chloroform  anesthesia,  in 
lightning  stroke,  and  as  a  sequel  to  auricular  fibrillation.  Death 
from  this  cause  is  usually  sudden,  and  is  preceded  by  disappear- 
ance of  the  radial  pulse,  and  by  an  electrocardiogram  recording 
complete  sequential  dissociation  of  the  ventricular  complexes. 

Alternation  Arhythmia. — This  represents  an  irregularity  in  the 
force  of  the  succeeding  cardiac  contractions,  without  deviation  of 
the  normal  incidence  of  the  beats,  and,  clinically,  accounts  for  the 
alternating  pulse  (pulsus  alternans),  in  which  the  beats,  although 
regular  in  rate  and  occurrence,  are  alternately  large  and  small. 
This  anomaly  depends  upon  variations  in  the  quantity  of  blood 
expelled  from  the  left  ventricle  by  its  alternately  strong  and  weak 
contractions,  and  is  explained  by  two  different  theories:  (a)  Incom- 
plete ventricular  systole,  owing  to  persistence  of  the  refractory 
period  in  a  circumscribed  area  of  the  ventricular  wall,  which  fails  to 
contract  while  the  other  part  of  the  muscle  does  so  with  enfeebled 
force  (Gaskell;  Hering);  and  (b)  general  ventricular  hyposystole, 
with  commensurately  weak  contractile  force  (Wenckebach). 
In  either  event  the  arterial  pulsations  are  alternately  strong  and 
weak  and  the  cardiac  sounds  correspondingly  loud  and  obscure. 
Usually,  sphygmocardiographic  tracings  more  clearly  show  the 
alternating  phases  of  this  type  of  arhythmia  than  the  curves  of  the 
electrocardiogram  (Gravier),  and  auscultatory  sphygmomanometry 
affords  distinctive  tonal  changes.  (See  p.  36.) 

Hemisystolic  Arhythmia. — This  extraordinarily  rare  disturbance 
is  characterized  by  asynchronous  ventricular  contractions,  or  hemi- 
systoles,  and  is  met  with  in  extreme  mitral  incompetence  associated 
with  excessive  intrapulmonary  hypertension.  As  the  result  of  this 
stress,  the  right  ventricle,  gorged  with  blood  and  greatly  overtaxed, 
makes  a  double  systole,  the  second  contraction  representing  an 
ineffectual  attempt  to  overcome  the  circulatory  stasis  in  the  pulmonary 
circuit.  By  this  mechanism  a  double  apical  first  sound  is  produced, 
the  second  element  of  which  is  loudest  over  the  right  ventricle;  a 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       371 

double  apex-beat  is  also  created,  but  there  is  only  a  single  arterial 
pulse-wave,  inasmuch  as  the  second  impulse,  being  that  of  the  right 
ventricle,  cannot  influence  the  systemic  blood-stream. 

Another  type  of  hemisystole,  excited  by  excessive  digitalization, 
consists  of  independent  contractions,  first  of  the  left  and  then  of  the 
right  ventricle,  this  peculiarity  having  been  attributed  to  the  com- 
paratively sluggish  reaction  of  the  right  ventricle  to  digitalis  and  to 
the  predominant  effect  of  the  drug  on  the  left  ventricle. 

Prolongation  of  Diastole. — Prolongation  of  the  second  or  long 
pause  after  the  second  sound  converts  the  physiologic  3-4  time  of 
the  cardiac  cycle  into  a  4-4  rhythm,  the  first  half  of  which  is  occu- 
pied by  the  first  and  second  sounds  and  the  last  half  by  the  dias- 
tolic  period  of  silence. 

In  this  form  of  arhythmia  both  the  first  and  second  sounds  are 
shorter  and  higher  pitched  than  normal,  and  become  approximated 
by  the  shortening  of  the  interval  between  them,  while  the  diastolic 
pause  is  sustained  through  fully  one-half  the  entire  cardiac  cycle. 
A  prolonged  diastole  is  suggestive  of  advanced  myocardial  disease, 
owing  to  which  the  ventricles,  exhausted,  ill-nourished,  and  tottering, 
have  become  almost  too  feeble  to  functionate;  the  sign  may  also  be 
symptomatic  of  digitalization. 

Embryocardia. — Unnatural  frequency  and  equidistant  spacing  of 
the  heart's  sounds,  from  prolongation  of  the  short,  and  abbreviation 
of  the  long,  pause,  is  termed  embryocardia.  As  the  name  suggests, 
it  resembles  the  regular  beating  of  the  fetal  heart,  in  that  the  two 
sounds  are  similar  and,  since  both  silences  are  of  equal  length,  follow 
each  other  at  regular  intervals,  like  the  tick-tack  of  a  watch. 

Embryocardia  means  striking  cardiac  enfeeblement,  by  fault  of 
which  the  ventricles  must  labor  hard,  slowly,  and  almost  fruitlessly 
to  expel  their  contents.  The  presence  of  this  sign  in  high-grade 
arterial  sclerosis,  in  primary  myocarditis,  and  during  the  acute 
infectious  fevers  generally  indicates  that  complete  heart  failure  is  not 
far  off. 

An  embryocardiac  tick-tack  may  also  be  associated  with  simple 
tachycardia,  in  which  event  it  is  to  be  referred  to  a  shortening  of  the 
long  pause.  Occurring  under  such  a  circumstance,  the  sign  is  not 
of  grave  import. 

Pendulum  Rhythm. — This  consists  of  a  succession  of  uniform  car- 
diac tones,  evenly  spaced,  equally  intense,  and  not  unduly  accelerated, 
in  consequence  of  which  peculiarities  the  regular  swing  of  a  pendulum 
is  more  or  less  faithfully  reproduced  by  the  heart's  two  sounds. 
This  anomaly  of  rhythm  is  met  with  in  conditions  of  arterial  hyper- 


372  PHYSICAL   DIAGNOSIS 

tension  wherein  ventricular  systole  is  prolonged  and  the  second 
sound  correspondingly  delayed,  at  the  expense  of  the  long  pause. 

ADVENTITIOUS  SOUNDS 

The  normal  cardiac  sounds,  in  addition  to  undergoing  rhythmic 
and  tonal  modifications,  are  also  attended,  if  not  wholly  replaced, 
by  certain  superadded,  adventitious  sounds  of  pathologic  significance, 
generated  within  the  cardiac  chambers  and  the  blood-vessels,  between 
the  pericardial  surfaces,  and  in  the  pulmonary  structures  contiguous 
to  the  heart.  These  abnormal  sounds,  for  simplicity's  sake,  may  be 
grouped  as — (a)  endocardial;  (b)  exocardial;  and  (c)  vascular.  Endo- 
cardial  murmurs,  or  bruits,  are  of  two  principal  types,  organic  and 
functional,  the  former  arising  from  unalterable  structural  defects 
of  the  cardiac  valves  and  orifices,  and  the  latter  depending  upon 
myocardial  enfeeblement  and  upon  changes  in  the  composition  of 
the  blood.  Exocardial  sounds  comprise  the  dry  rub  of  pericardial 
friction,  the  splash  of  the  pericardial  succussion  sound,  and  the  whiff 
of  the  cardiopulmonary  murmur;  other  extracardiac  sounds,  primarily 
of  pleural  and  pulmonary  origin,  include  pleuropericardial  friction 
and  cardiopneumatic  rales,  the  mechanism  and  meaning  of  which 


thd 


Systole.  Diastole. 

Fig.  147. — Mechanism  of  normal  cardiac  systole  and  diastole. 

have  been  explained  in  another  place.  (See  p.  166  et  seq.)  Vascular 
adventitious  sounds  are  classified  as  either  arterial  or  venous,  according 
to  their  seat  of  origin,  and  of  these  sounds,  the  aneurismal  bruit  and 
the  venous  hum  are  the  most  important  clinical  examples. 

ENDOCARDIAL   MURMURS 

Organic  Murmurs. — No  sound  whatever,  save  the  lup  of  the 
first,  and  the  dup  of  the  second,  cardiac  tone,1  attends  the  passage  of 

1  Practically,  the  so-called  "  third  heart-sound,"  referred  to  on  page  357, 
can  be  disregarded  in  routine  examinations. 


EXAMINATION   OF   THE    CARDIOVASCULAR   SYSTEM       373 

blood  through  the  normal  heart,  since  a  column  of  blood  coursing, 
at  a  normal  velocity,  through  healthy  endocardiac  orifices  and 
chambers  does  so  without  the  formation  of  the  current  oscillations 
essential  for  the  generation  of  murmurs.  In  other  words,  a  normal 
endocardiac  circulation  is  comparable,  physically,  to  the  flow  of  fluid 
through  a  tube  of  uniform  caliber,  and  having  smooth  walls  separated 
from  the  current  by  a  film  of  liquid  attached  to  them  by  the  force  of 
adhesion;  under  such  conditions  the  smooth,  uniform,  silent  flow  of 
the  fluid  is  assured.  When,  on  the  other  hand,  structural  deformi- 
ties of  the  valves  and  orifices  exist,  the  blood-stream  is  churned  into 

Stenotic.  Regurgitant. 


Fig.  148. — Mechanism  of  stenotic  and  regurgitant  murmurs. 

sonorous  vibrations,  just  as  fluid  passing  through  a  tube  swirls  about 
and  is  hurled  into  tiny  jets  should  it  be  forced  through  a  constriction 
of  the  tube's  lumen  into  an  expanded  portion  beyond.  An  orifice 
organically  contracted  and  therefore  obstructing  the  onward  move- 
ment of  the  blood-stream  (stenosis) ,  or  an  opening  deformed  so  as  to 
allow  the  blood  to  leak  backward  (regurgitatiori)  results,  in  either 
accident,  in  the  passage  of  the  stream  into  a  larger  cavity,  already 
containing  blood,  and  in  consequence  blood  eddies  and  vibratory  jets 
termed  fluid  veins  (Savart's  veines  fluides)  are  produced  (Fig.  148). 
These  sonorous  vibrations  are  conducted,  with  variable  intensity,  by  the 
cardiac  muscle  and  thoracic  parietes  to  the  surface  of  the  chest,  where 
they  are  audible  as  murmurs  (bruit;  souffle)  and  palpable  as  thrills. 
Inasmuch  as  a  sluggish  current  of  blood  is  not  readily  thrown  into 
sonorous  vibrations,  despite  the  existence  of  deformed  orifices  and 
valves,  the  blood-stream  must  attain  a  certain  degree  of  velocity  in 
order  to  generate  audible  murmurs,  in  view  of  which  the  intensity 
of  a  given  murmur  indicates  the  condition  of  the  circulatory  force 
and  does  not,  per  se,  denote  the  extent  or  gravity  of  an  endocardial 
lesion.  To  some  extent  blood  viscosity  bears  upon  the  production 
of  murmurs,  both  organic  and  functional,  since  hypoviscosity  and 


374 


PHYSICAL   DIAGNOSIS 


undue  dilution  of  the  blood-mass  favor  the  creation  of  vibrations 
therein.  Matsuo  finds  that  anemic  murmurs,  whose  intensity  is 
inversely  proportional  to  the  blood's  viscosity  value,  disappear 
when  this  figure  exceeds  3.0. 

Clinical  Attributes  of  Murmurs. — Having  detected  a  murmur, 
it  is  next  in  order  to  determine  its  relation  to  the  events  of  the  cardiac 
cycle,  its  point  of  maximum  precordial  intensity  and  lines  of  trans- 
mission therefrom,  and  its  quality,  intensity,  and  other  tonal  charac- 
teristics. By  this  sort  of  analysis  one  attempts  to  decide  whether 
the  murmur  is  simply  a  functional  accident  or  is  a  sign  of  endocardial 
disease,  and  if  the  latter  be  the  finding,  to  discover  the  anatomic  site, 
nature,  and  extent  of  the  lesion,  as  well  at  its  effect  upon  the  structure 
and  adequacy  of  the  heart.  In  this  inquiry  the  foregoing  data  are 
invariably  to  be  correlated  with  signs  relating  to  the  size  and  position 


Systolic 


Diastolic 


Presystolic 


Fig.  149. — The  rhythm  or  time  of  murmurs. 

of  the  heart,  to  the  character  of  the  cardiac  tones  audible  at  the  four 
valve  areas,  and  to  the  condition  of  the  arterial  and  venous  circula- 
tions. 

The  Rhythm  of  Murmurs. — Endocardial  murmurs  correspond 
definitely  to  the  events  of  the  cardiac  cycle,  and  occur  during  ven- 
tricular systole,  ventricular  diastole,  and  auricular  systole  (Fig.  149). 
The  ventricular  systole  and  diastole  are  taken  as  the  clinical  time- 
criteria  of  murmurs,  those  occurring  with  systole,  accompanying  or 
replacing  the  first  sound,  being  termed  systolic,  those  coincident 
with  diastole,  blending  with  or  masking  the  second  sound,  being 


EXAMINATION    OF   THE    CARDIOVASCULAR    SYSTEM       375 

known  as  diastolic;  and  those  audible  immediately  before  systole 
being  called  presystolic.  A  post-systolic  murmur  is  audible  toward 
the  end  of  systole;  a  protodiastolic  murmur  occurs  in  the  earliest  part 
of  diastole,  directly  after  the  first  sound;  and  a  mid-diastolic  mumur 
corresponds  to  the  middle  of  the  diastolic  period. 

Murmurs  are  timed  by  determining  their  relation  to  the  sounds 
of  the  heart,  the  visible  apex-beat,  or  the  palpable  carotid  pulsa- 
tion; the  radial  pulse  is  not  a  correct  index  of  ventricular  systole,  than 
which  the  pulse-wave  at  the  wrist  is  appreciably  later. 

Puncta  Maxima  and  Transmission  of  Murmurs. — An  organic 
murmur  is  usually  heard  most  distinctly  over  the  precordial  valve 
area  corresponding  to  its  seat  of  production,  this  site  being  known  as 
the  punctum  maximum,  or  point  of  maximum  intensity.  Further- 
more, if  audible  beyond  this  limit,  a  murmur  tends  to  be  conducted 
selectively  along  a  restricted  path  termed  its  line  of  transmission,  or 
area  of  propagation.  The  puncta  maxima  and  transmission  line? 
of  different  murmurs  will  be  considered  in  detail  later,  but  in  general 
terms  it  may  be  here  stated  that  the  former  are  situated  where  the 
murmurous  orifice  lies  closest,  acoustically,  to  the  surface  of  the 
thorax,  and  that  the  course  of  the  latter  is  determined  both  by  the 
direction  of  the  blood-current  and  by  the  conducting  properties  of 
the  structures  lying  between  the  source  of  the  vibrations  and  the 
chest-piece  of  the  examiner's  stethoscope.  The  initial  intensity  of 
the  bruit,  its  quality  and  pitch,  and  the  velocity  of  the  blood-stream 
are  also  to  be  taken  into  account  as  determining  factors  of  a  murmur's 
extraprecordial  transmission. 

The  Intensity  and  Quality  of  Murmurs. — Like  the  normal  heart- 
sounds,  the  distinctness  of  murmurs  is  modified  by  posture,  as 
well  as  by  the  conducting  properties  of  the  thorax  and  contiguous 
parts.  The  acoustic  characters  and  intensity  of  a  murmur  vary 
greatly,  depending  as  they  do  upon  the  force  of  the  blood-current 
and  upon  the  extent  and  nature  of  the  underlying  lesion,  the  gravity 
of  which  can  by  no  means  be  judged  by  criteria  such  as  loudness  and 
tonal  attributes.  However,  generally  speaking,  a  loud  murmur 
means  that  the  heart  is  well  nourished  and  acting  adequately,  while, 
on  the  other  hand,  a  feeble  murmur  suggests  that  the  heart  is  weak, 
if  not  failing.  This  dictum  is  especially  true  when  applied  to  an 
instance  in  which  a  murmur,  once  loud,  bellows-like,  and  accom- 
panied by  a  thrill,  dwindles  to  a  mere  whiff,  unaccompanied  by  the 
slightest  tactile  vibrations. 

Progressive  increase  in  the  intensity  of  a  murmur  generally  implies 
that  the  cardiac  strength  is  correspondingly  improved.  Some 


376  PHYSICAL   DIAGNOSIS 

murmurs  are  so  loud  as  to  be  heard  distinctly  by  the  patient,  and 
others  are  so  intense  that  they  can  be  recognized  by  a  bystander. 
A  systolic  or  a  diastolic  murmur  may  simply  blend  with  the  first 
or  second  sound  of  the  heart,  and  thus  modify  its  normal  quality, 
or  it  may  be  so  loud  as  totally  to  obscure  it,  and  the  greater  this 
replacement  of  the  physiologic  heart-sounds  by  the  murmur,  the 
more  extensive  the  valve  defect  is  likely  to  be.  Thus,  a  distinct  first 
sound  plus  a  systolic  murmur  at  the  apex  means  that  the  mitral  valve 
is  not  so  crippled  that  it  cannot  close,  though  it  may  do  so  imperfectly; 
and,  similarly,  a  persistent  second  sound  with  a  diastolic  murmur 
in  the  aortic  area  shows  that  the  competency  of  the  aortic  leaflets 
is  not  totally  abolished. 

With  reference  to  quality  and  pitch,  a  murmur  may  be  described 
as  soft,  distant,  and  blowing;  or  rough,  harsh,  filing,  and  rasping; 
or  rumbling,  churning,  and  blubbering.  Such  adjectives  as  these, 
though  by  no  means  certain  keys  to  the  source  of  an  endocardial 
murmur,  have  within  certain  limits  a  pertinent  clinical  bearing.  For 
example,  the  typical  mitral  presystolic  murmur  is  loud  and  rumbling 
or  blubbering;  the  systolic  mitral  murmur,  on  the  contrary,  is  generally 
soft  and  quiet  and  blowing.  The  systolic  aortic  murmur  is  usually 
loud,  harsh,  and  rasping;  but  the  diastolic  murmur  in  this  area  is 
likely  to  be  distant  and  subdued,  if  not,  indeed,  almost  noiseless. 
These  facts  apply,  of  course,  only  to  the  characteristic  case,  to  which 
exceptions  are  not  uncommon. 

The  pitch  of  a  murmur  is  likewise  a  most  variable  quality,  being 
low  and  sonorous  in  some  instances,  and  high  and  sharp  in  others. 
Like  other  bruits,  a  musical  murmur,  or  one  having  a  musical 
twang  or  plaintive  tone,  may  be  due  to  the  vibrations  of  blood- 
eddies,  but  frequently  it  is  produced  by  the  fenestration  of  a  valve, 
or  by  the  vibrations  of  thickened  chordae  tendineae,  of  a  delicate 
thread  of  fibrin,  or  of  the  thin  free  edge  of  a  valve  leaflet.  Accord- 
ing to  Cldment,  increased  rapidity  of  the  intracardiac  blood-flow 
is  an  important  factor  of  the  musical  quality.  Obviously,  a 
musical  murmur,  per  se,  points  to  no  single  type  of  endocardial 
defect.  Metallic,  amphoric,  echoing  murmurs  arise  from  the  same 
conditions  that  lend  these  tonal  qualities  to  the  normal  heart-sounds, 
the  nature  of  which  has  already  been  discussed. 

Peculiarities  of  quality  and  pitch  are  to  be  carefully  noted  when 
attempting  to  differentiate  the  adventitious  sounds  afforded  by  a 
heart  tenanted  by  multiple  murmurs,  which,  though  audible  at  the 
same  periods  of  the  cardiac  cycle,  may  differ  radically  in  tone. 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       377 

Functional  Murmurs. — These  bruits,  like  those  of  organic 
origin,  are  due  to  sonorous  vibrations  of  the  circulating  blood-stream, 
but,  unlike  them,  they  do  not  depend  upon  permanent  structural 
defects  of  the  valve  mechanism.  To  this  sort  of  murmurs  the 
adjectives  inorganic,  relative,  accidental,  and  hemic  are  also  applied, 
for  they  are  produced  by  temporary  myocardial  weakness  whereby 
the  action  of  the  valves  is  disarranged,  or  by  dilatation  of  the  conus 
arteriosus,  or  of  the  pulmonary  artery.  Diminished  blood  density,  as 
mentioned  above,  contributes  to  the  causation  of  functional  murmurs, 
inasmuch  as  thinning  of  the  blood  favors  the  formation  of  eddies 
and  jets  in  the  circulating  stream.  Anemia,  acute  febrile  affections, 
and  extreme  physical  exhaustion  are  the  principal  factors  of  func- 
tional murmurs,  of  which  the  hemic  bruit  of  chlorosis,  the  relative 
mitral  incompetence  of  various  specific  fevers,  and  the  relative 
tricuspid  leakage  consequent  to  excessive  intrapulmonary  tension 
are  familiar  examples.  The  presystolic  murmur  of  Flint,  met  with 
in  aortic  regurgitation,  is  also,  in  a  certain  sense,  relative  or  func- 
tional. (See  p.  382.) 


III.  Tricuspid  and  aortic ^JB  {"")    (~)  j^ft- 1.  Pulmonic 


H.  Mitral 


Fig.  150. — Comparative  incidence  of  functional  murmurs  of  the  different  valve  areas. 

(Cf.  Fig.  152.) 

Functional  murmurs,  in  their  order  of  relative  frequency,  are 
audible  at  the  pulmonic,  mitral,  tricuspid,  and  aortic  valve  areas, 
and  in  the  vast  majority  of  cases  are  systolic  in  time,  faint  and  blowing 
in  quality,  and  not  conducted  far  beyond  the  precordia,  though 
within  this  area  they  may  imitate  the  transmission  lines  of  organic 


PHYSICAL  DIAGNOSIS 

murmurs  similarly  timed  and  situated.  Functional  murmurs  are 
not  productive  of  cardiac  hypertrophy,  of  distinctive  pulse  changes, 
or  of  consecutive  alterations  in  the  basic  sounds  of  the  heart.  They, 
furthermore,  have  a  transient,  fleeting  character,  for  they  disappear 
with  the  removal  of  their  exciting  cause — when  the  blood-count 
improves,  after  the  fever  declines,  or  with  the  subsidence  of  the 
heart  stress,  as  the  case  may  be.  A  functional  murmur  of  purely 
anemic  character  is  ordinarily  accompanied  by  a  venous  hum 
(q.  v.). 

The  mechanism  of  functional  murmurs  is  probably  not  identical 
in  all  instances.  The  pidmonic  systolic  bruit  of  anemic  states, 
especially  chlorosis,  is  best  explained  by  assuming  nutritional  weak- 
ness of  the  myocardium,  whereby  the  conus  arteriosus  dilates  and 
leads  to  the  formation  of  fluid  veins  within  this  portion  of  the  right 
ventricle.  The  pulmonic  area  is  also  the  site  of  an  evanescent 
systolic  murmur  of  functional  type,  occurring  in  emotional  women, 
and  termed  the  "psychic  heart  murmur."  An  apical  systolic 
murmur,  of  transient  duration,  develops  in  many  infectious  dis- 
eases in  consequence  of  toxic  degeneration  of  the  myocardium. 
This  induces  stretching  of  the  left  ventricle,  undue  enlargement  of 
the  mitral  ring,  and  relative  shortening  of  the  papillary  muscles, 
by  fault  of  which  defects  the  mitral  valve  fails  to  close  tight  during 
the  ventricular  contraction,  and  therefore  permits  the  leakage  of 
blood  from  the  ventricle  into  the  auricle  with  each  systole  (Fig.  151). 
This  murmur  of  ''relative"  or  "accidental"  mitral  incompetence 
disappears  as  the  patient  convalesces  and  the  heart  muscle  regains 
its  normal  tone.  A  murmur  of  similar  mechanism  is  frequently 
audible  at  the  apex  for  a  very  brief  period  as  a  consequence  of 
physical  exercise  severe  enough  to  throw  undue  strain  upon  the  left 
ventricle,  by  provoking  excessive  systemic  arterial  tension.  Other 
murmurs,  timed  similarly,  are  audible  at  the  apex  as  the  result  of 
the  formation  of  audible  blood-eddies  within  a  dilated  left  ventricle, 
without  leakage  at  the  mitral  orifice.  A  systolic  tricuspid  mur- 
mur, of  relative  type,  may  arise  as  the  result  of  valvular  dis- 
ease of  the  left  heart,  whereby  excessive  intrapulmonary  arte- 
rial tension  is  set  up,  thus  dilating  the  right  ventricle,  and,  by 
enlarging  the  tricuspid  orifice,  allowing  tricuspid  leakage.  This 
so-called  "safety-valve"  murmur  is  really  conservative,  in 
that  for  the  time  it  eases  the  high  pressure  within  the  right  ven- 
tricle. (See  p.  463.)  Relative  tricuspid  regurgitation  may  also 
attend  the  obstinate  obstruction  of  the  pulmonary  circuit  accom- 
panying certain  chronic  pulmonary  affections.  An  aortic  func- 


EXAMINATION    OF    THE    CARDIOVASCULAR   SYSTEM        379 

tional  murmur,  if  systolic,  probably  means  dilatation  of  the  left 
ventricle  without  stretching  of  the  aortic  ring,  or,  in  other  words, 
relative  stenosis  of  the  aortic  orifice;  or  transient  dilatation  of  the 
aorta  may  be  the  exciting  cause  of  a  systolic  aortic  bruit.  The 
exceedingly  rare  diastolic  functional  murmur  audible  at  the  aortic 
area  is  best  explained  by  assuming  it  to  be  the  diastolic  element 
of  a  venous  hum  (q.  t>.)  conducted  from  the  jugular  veins  down- 
ward into  the  superior  vena  cava. 


Fig.  151. — Mechanism  of  a  functional  murmur  due  to  ventricular  dilatation: 
I,  Normal  systolic  coaptation  of  auriculoventricular  leaflets;  II,  incompetence  due  to 
relative  shortening  of  papillary  muscles  (chamber  elongated);  III,  incompetence  due 
to  enlargement  of  mitral  ring  (chamber  stretched  horizontally). 

The  differentiation  of  organic  and  functional  cardiac  murmurs  is 
generally  possible,  when  all  the  clinical  findings  are  given  due  weight, 
though  in  some  instances  one  must  withhold  a  definite  decision,  at 
least  temporarily.  For  example,  the  apical  systolic  murmur  so 
commonly  arising  in  acute  rheumatic  fever  may  be  symptomatic 
either  of  endocarditis,  myocardial  relaxation,  or  high-grade  anemia 
due  to  the  action  of  the  rheumatic  toxin,  and  under  such  a  circum- 
stance one  cannot  venture  an  opinion  as  to  the  character  of  the 
murmur  until  some  time  has  elapsed — sufficient  for  the  murmur  to 
disappear,  if  functional,  or  for  it  to  become  supplemented  by  corrobo- 
rative signs,  if  organic.  The  following  table  may  prove  helpful  in 


380 


PHYSICAL   DIAGNOSIS 


emphasizing  the  main  points  of  difference  between  these  two  types 
of  endocardial  sounds. 


Time: 

Punctum  maximum: 

Transmission: 

Myocardium: 

Pulse: 
Anemia: 
Previous  history: 

Basal  cardiac  sounds: 
Duration: 


ORGANIC. 

Systolic,  diastolic,  or 
presystolic. 

Varies  with  site  of 
valve  lesion. 

Conducted  select- 
ively or  circum- 
scribed. 

Permanent  struc- 
tural changes. 

Often  distinctive. 
Not  a  factor. 

Endocarditis,  pro- 
longed muscular 
strain,  habitual 
arterial  hyper- 
tension. 

Generally  show  dis- 
tinctive changes. 

Permanent. 


FUNCTIONAL. 

Almost       invariably 

systolic. 
Usually  at  pulmonic 

area. 
Rarely        conducted 

beyond  precordia. 

Heart  not  perma- 
nently altered  in 
structure. 

No  characteristic 
change. 

Frequently  an  im- 
portant factor. 

No  history  of  organic 
endocardial  dis- 


No        characteristic 

modifications. 
Transient. 


The  Analysis  of  Murmurs. — The  particular  defect  indicated  by 
a  given  endocardial  murmur  is  ascertained  by  carefully  analyzing 
the  several  attributes  of  the  sound,  and  by  correlating  these  data 
with  a  clear  conception  of  the  physical  condition  of  the  murmurous 
valve  and  orifice  at  the  precise  moment  the  sonorous  vibrations  are 
heard.  The  four  different  valve  areas  and  transmission  paths 
leading  therefrom,  therefore,  are  to  be  auscultated  systematically, 
the  examiner  meanwhile  being  guided  by  these  cardinal  clues  to  the 
identity  of  organic  murmurs  in  general :  that  at  the  mitral  and  tri- 
cuspid  areas  systolic  murmurs  mean  incompetence,  and  presystolic 
murmurs,  obstruction,  of  the  auriculoventricular  orifice;  that  at  the 
aortic  and  pulmonic  areas  systolic  murmurs  indicate  obstruction, 
and  diastolic  murmurs,  incompetence,  of  the  arterial  outlet  of  the 
ventricle;  and  that,  as  a  rule,  the  bruits  of  obstruction  are  intense  and 
harsh  and  clear  cut,  while  those  of  incompetence  are  relatively 
feeble  and  soft  and  indistinct. 

With  these  facts  in  mind,  it  is  convenient  to  investigate  the  individ- 
ual murmurs  heard  over  the  precordia  according  to  their  relation  to 
the  four  auscultatory  sites  thereupon.  More  detailed  consideration, 
pathologic  and  clinical,  of  the  individual  endocardial  lesions  whereby 
murmurs  are  generated  is  given  in  Section  VI.  (See  p.  427.) 


EXAMINATION   OF   THE    CARDIOVASCULAR    SYSTEM       381 


II.  Aortic- 


^— IV  Pulmonic 
III.  Tricuspid 
I.  Mitral 


Fig.  152. — Comparative  incidence  of  organic  murmurs  at  the  different  valve  areas. 

(Cf.  Fig.  150.) 


Fig.  153. — The  mitral  presystolic  murmur. 

Mitral  Murmurs. — Murmurs  due  to  lesions  of  the  mitral  orifice 
may  be  of  either  presystolic  or  systolic  rhythm,  the  former  being 


382  PHYSICAL   DIAGNOSIS 

audible  just  before  the  cardiac  first  sound  and  indicating  obstruction, 
and  the  latter  being  synchronous  with  the  first  sound  and  signifying 
incompetence. 

Mitral  Presystolic  Murmurs. — Mitral  stenosis  accounts  for  an 
apical  murmur  produced  by  contraction  of  the  left  auricle,  whereby 
the  blood-stream  is  churned  into  sonorous  vibrations  as  it  is  forced 
through  a  constricted  auriculoventricular  orifice  into  the  ventricle. 
The  rhythm  of  this  murmur  corresponds  to  the  end  of  ventricular 
diastole,  at  which  period  the  auricle's  contractile  force  and  the 
velocity  of  the  blood-current  are  greatest;  less  commonly,  it  occurs 
earlier  in  the  diastolic  period,  in  which  case  the  vibrations  depend 
more  upon  the  suction  action  of  the  ventricle,  which  is  most  powerful 
at  the  beginning  of  diastole,  than  upon  the  driving  force  of  the  auricle. 

The  mitral  stenotic  murmur  has  its  punctum  maximum  just  above 
and  within  the  apex  of  the  heart,  is  virtually  not  transmitted  thence, 
and  is  usually  accompanied  by  a  distinct  apical  presystolic  thrill 
(Fig.  153).  In  its  typical  form  the  murmur  is  loud,  harsh,  and 
ingravescent  or  crescendo  (i.  e.,  gradually  increasing  in  loudness 
as  it  progresses),  and  terminates  in  a  sharp,  snappy  first  sound; 
less  commonly,  it  is  quiet  and  soft,  as  in  the  "suction  force  mur- 
mur" of  the  early  phase  of  diastole.  Disappearance  of  the  bruit, 
in  that  it  indicates  failing  power  of  the  left  auricle,  is  of  unfavor- 
able import.  Associated  signs  of  mitral  obstruction  include  ac- 
centuation and  reduplication  of  the  pulmonic  second  sound,  and 
doubling  of  the  apical  second  sound.  Mitral  incompetence  and 
obstruction  frequently  coexist,  and  ultimately  tricuspid  incompe- 
tence may  supervene,  in  consequence  of  the  stress  imposed  upon 
the  right  ventricle. 

The  presystolic  Flint  murmur  of  aortic  regurgitation  is  audible  in 
the  mitral  area  to  which  it  is  practically  restricted.  For  its  production 
dilatation  of  the  left  ventricle  and  incompetence  of  the  aortic  valve 
are  regarded  as  the  essential  factors.  Owing  to  the  enlargement  of 
the  ventricular  cavity,  the  anterior  cusp  of  the  mitral  valve  is  dis- 
placed, during  diastole,  from  its  accustomed  mural  position,  so  that 
it  projects  into  the  rising  tide  of  blood  within  the  ventricle,  and 
consequently  becomes  the  target  of  two  blood-streams  coming  from 
opposite  directions — one  regurgitating  through  a  leaky  aortic  orifice 
and  the  other  issuing  (normally)  from  the  mitral  opening.  By  this 
mechanism  vibrations  of  the  cusp  are  set  up  toward  the  middle  or 
end  of  diastole,  with  the  generation  of  a  presystolic  murmur  and 
thrill  appreciable  at  the  apex.  Flint's  murmur  lacks  the  sharp 
apical  first  sound  and  the  intense  ingravescence  of  the  bruit  of  true 


EXAMINATION    OF    THE    CARDIOVASCULAR    SYSTEM       383 


mitral  stenosis,  and,  moreover,  is  invariably  associated  with  the 
lesion  of  aortic  regurgitation  (q.  v.). 

A  pericarditic  presystolic  rumble  is  occasionally  audible  at  and  for 
some  distance  above  the  apex,  in  subjects  of  plastic  pericarditis, 
especially  in  children.  It  is  most  likely  that  this  sound  represents 
an  auriculosystolic  (presystolic)  friction-rub,  symptomatic  of  peri- 
cardial  adhesion;  it  is  attended  by  none  of  the  valvular  tonal  changes 
peculiar  to  the  bruit  of  mitral  stenosis  of  the  organic  type  (q.  i;.). 

Mitral  Systolic  Murmurs. — Mitral  regurgitation  is  responsible  for 
the  vast  majority  of  all  systolic  murmurs  audible  at  the  apex  of  the 
heart,  the  sound  betraying  incompetence  of  the  left  auriculoventric- 
ular  orifice,  by  fault  of  which  each  contraction  of  the  left  ventricle 
forces  a  part  of  its  contained  blood  backward  into  the  left  auricle. 
The  murmur  thus  produced  blends  with  or  masks  the  first  cardiac 
sound,  is  commonly  of  a  blow- 
ing character,  and  from  its 
apical  punctum  maximum  is 
transmitted  toward  the  left 
axilla  and  sometimes  to  the 
left  scapular  angle  by  the 
continuous  pathway  of  con- 
duction formed  by  the  ante- 
rior papillary  muscles  and  the 
ventricular  wall  (Fig.  154). 
Accentuation  of  the  pulmonic 
second  sound  is  an  important 
concomitant  sign  of  this  de- 
fect, which,  as  stated  else- 
where, may  be  due  to  endo- 
carditic  or  sclerotic  changes, 
or  purely  to  ventricular  re- 
laxation, leading  to  disparity 
between  the  size  of  the  mitral 
opening  and  of  the  valve- 
leaflets  that  should  guard  it. 
It  is  well  to  remember  that 
functional  murmurs  of  mitral  regurgitation  vanish  when  the  cardiac 
tone  improves  sufficiently  to  allow  the  mitral  opening  to  resume 
its  normal  diameter,  but  that  murmurs  of  organic  mitral  leakage 
are  prone  to  become  louder  when  the  force  of  the  heart  increases. 

Aortic  Murmurs. — Both  systolic  and  diastolic  murmurs  are 
audible  in  the  aortic  area  in  consequence  of  disease  of  the  aortic 


Fig.  154 — The  mitral  systolic  murmur. 


PHYSICAL    DIAGNOSIS 


valve,  those  accompanying  the  first  sound  indicating  obstruction, 
and  those  synchronous  with  the  second  sound,  incompetence.  Aortic 
systolic  murmurs  are  more  frequently  due  to  sclerotic  roughening 
and  to  dilatation  of  the  aorta  than  to  actual  constriction  of  the  orifice, 
while,  less  commonly,  a  systolic  bruit  in  the  aortic  region  means 
aneurism. 

Aortic  Systolic  Murmurs. — True  aortic  stenosis  causes  a  loud,  harsh 
murmur  at  the  aortic  cartilage,  the  sound  being  transmitted  thence 
into  the  arteries  of  the  neck  (Fig.  155).  In  typical  instances  the  mur- 

^^m  mur  is  accompanied  by  a 
coarse  thrill  and  the  aortic 
second  sound  is  notably  en- 
feebled. Organic  narrowing 
of  the  aortic  orifice,  at  which 
fluid  veins  are  agitated  by 
each  ventricular  systole,  ex- 
plains the  mechanism  of  this 
bruit,  which  rarely  exists  as  an 
isolated  lesion. 

Aortic  roughening,  by  all 
odds  the  commonest  defect  in 
this  region,  provokes  a  mur- 
mur of  the  same  rhythm,  site, 
and  propagation  as  that  of 
genuine  stenosis,  but  it  is  not 
so  frequently  associated  with 
a  thrill,  and  the  aortic  second 
sound  is  loud,  clear,  and 
ringing.  The  mechanism  of 
this  bruit  is  shown  by  Fig. 

163- 

Dilatation  of  the  aorta,  producing  a  relative  stenosis  of  the  aortic 
orifice,  and  aneurism  of  the  aortic  arch  produce  systolic  aortic  mur- 
murs, but  in  a  dilated  aorta  one  expects  to  find  a  corresponding  area 
of  local  dulness,  as  well  as  an  accentuated  aortic  second  sound; 
while  in  aneurism  there  is  usually  no  difficulty  in  discovering  dis- 
tinctive evidences  of  an  aneurismal  tumor.  (See  Fig.  163.) 

Aortic  Diastolic  Murmurs. — Almost  invariably  these  are  symp- 
tomatic of  aortic  re  gurgitation,  whereby  the  blood-column  within 
the  aorta  falls  backward,  during  ventricular  diastole,  through  an 
organically  incompetent  orifice,  and  in  so  doing  sets  up  a  prolonged 
soft  diastolic  murmur,  best  heard  at  or  below  the  aortic  cartilage, 


Fig.  155. — The  aortic  systolic  murir 


EXAMINATION    OF   THE    CARDIOVASCULAR    SYSTEM       385 


and  propagated  down  the  sternum  and  toward  the  apex  or  the  left 
axilla.  The  five  possible  puncta  maxima  of  this  murmur  are  shown 
in  the  accompanying  illustration  (Fig.  156).  Striking  hypertrophy, 
and  later  dilatation,  of  the  left  ventricle  develops  in  consequence  of 
this  lesion.  Relative  aortic  in- 
competence is  recognized  by 
the  presence  of  a  diastolic 
aortic  murmur  like  that  of 
an  organic  regurgitation,  and 
by  the  absence  of  the  other 
hall-marks  of  the  latter  con- 
dition; relative  leakage  is, 
furthermore,  attended  by  well- 
defined  evidences  of  left  ven- 
tricular dilatation  and  of  en- 
largement of  the  ascending 
portion  of  the  aortic  arch. 
That,  exceptionally,  a  diastolic 
anemic  bruit  may  be  clearly 
audible  in  the  aortic  area  is 
a  fact  worth  recalling. 

Tricuspid  Murmurs. — The 
tricuspid  area  affords  both  pre- 
systolic  (stenotic)  and  systolic 
(regurgitant)  murmurs,  gener-        Fig.  156.— The  aortic  diastolic  murmur. 
ated  by  a  mechanism  directly 

akin  to  that  of  corresponding  adventitious  sounds  at  the   mitral 
orifice. 

Tricuspid  Presystolic  Murmurs. — The  punctum  maximum  of  this 
extremely  rare  murmur,  which  never  means  anything  but  tricuspid 
obstruction,  is  at  the  base  of  the  ensiform  cartilage,  either  near  the 
middle  or  along  either  border  of  the  sternum,  whence  it  is  not  con- 
ducted (Fig.  157).  The  murmur  is  like  that  of  its  mitral  counterpart, 
both  rhythmically  and  acoustically,  and  not  uncommonly  is  accom- 
panied by  a  presystolic  thrill  and  by  enfeeblement  of  the  pulmonic 
second  sound  of  the  heart.  A  tricuspid  presystolic  murmur  ordinarily 
signifies  an  acquired  stenosis,  though  it  may  represent  a  congenital 
defect,  either  developmental  or  endocarditic. 

Tricuspid  Systolic  Murmurs. — A  tricuspid  systolic  murmur  may 
be  either  circumscribed  to  its  punctum  maximum  or  conducted 
therefrom  toward  the  right  and  upward  (Fig.  158).     Jugular  pul- 
sation of  the  ventricular  or  systolic  type,  hepatic  pulsation,  and 
25 


386 


PHYSICAL   DIAGNOSIS 

**Nk 

'9 


•  Fig.  157. — The  tricuspid  presystolic  murmur. 


Fig.  158. — The  tricuspid  systolic  murmur. 

weakening  of  the  pulmonic  second  sound  are  the  important  corrobora- 
tive signs  of  this  murmur  of  tricuspid  leakage.    This  lesion  is  a  very 


EXAMINATION    OF   THE    CARDIOVASCULAR   SYSTEM         387 

common  consequence  of  right  ventricular  dilatation,  and,  with  less 
frequency,  results  from  endocarditic  deformity  of  the  valve;  in  a 
limited  proportion  of  cases  the  murmur  is  of  anemic  origin. 

Pulmonic  Murmurs. — Organic  murmurs  having  their  punctum 
maximum  at  the  pulmonic  area,  like  those  of  aortic  origin,  are  either 
systolic  and  stenotic,  or  diastolic  and  regurgitant.  Such  murmurs 
are  extraordinarily  rare,  though,  as  mentioned  above,  anemic  bruits 
at  the  pulmonic  orifice  are  not  at  all  uncommon. 

Pidmonic  Systolic  Murmurs. — Exceptionally,  a  congenital  stenosis 
of  the  pulmonic  orifice  exists,  to  account  for  a  harsh  systolic  murmur, 


Fig.  159. — The  pulmonic  systolic  murmur. 

most  intense  at  the  pulmonic  orifice  and  conducted  upward  toward 
the  clavicle,  or,  if  very  intense,  spreading  over  the  upper  left  thoracic 
wall  (Fig.  159).  Impurity  or  suppression  of  the  pulmonic  second 
sound  is  a  convincing  attendant  sign,  and  usually  there  is  cyanosis, 
with  more  or  less  definite  auscultatory  evidences  of  other  congenital 
cardiac  defects,  notably  a  pervious  interventricular  septum. 

In  addition  to  the  pulmonic  systolic  murmurs  of  anemia  and  of 
organic  constriction,  similar  sounds  may  arise  from  relative  stenosis 
of  the  orifice,  created  by  dilatation  of  the  pulmonary  artery  imme- 
diately distal  to  its  ventricular  mouth,  but  in  this  condition  the 


388  PHYSICAL   DIAGNOSIS 

murmur,  which  is  likely  to  be  soft  and  quiet,  persists  only  so  long  as 
the  arterial  relaxation  producing  it  lasts,  and  the  patient  is  not 
cyanotic,  but  debilitated  and  poorly  nourished. 

In  auscultating  the  pulmonic  region  one  must  not  forget  that  this 
is  the  favorite  site  of  a  cardiorespiratory  murmur,  and  that  here  also 
may  be  heard  the  bruits  of  pulmonary  artery  stenosis,  of  aneurism, 
and  of  a  patent  interventricular  septum.  In  Section  VI.  the  differen- 
tiation of  these  puzzling  systolic  murmurs  is  dealt  with  individually. 

Pulmonic  Diastolic  Murmurs. — Organic  pulmonary  regurgitation 
is  a  clinical  curiosity  giving  rise  to  a  diastolic  murmur  of  maximum 


' 


Fig.  160. — The  pulmonic  diastolic  murmur. 

intensity  at  the  pulmonic  area,  and  transmitted  thence  downward 
and  sometimes  toward  the  mitral  region  (Fig.  160).  Also  of  rare 
occurrence  is  the  diastolic  murmur  of  relative  pulmonary  incompe- 
tence, or  of  leakage  from  stretching  of  the  pulmonic  ring  incident  to 
excessive  pressure  within  the  pulmonary  artery.  Aortic  regurgitant 
murmurs  are  distinguishable  only  by  a  process  of  exclusion  from  these 
similarly  timed  murmurs  of  pulmonary  regurgitation  (q.  v.  i.). 

Multiple  Murmurs. — In  organic  disease  of  the  endocardium 
two  or  more  murmurs  are  commonly  generated,  owing  to  the 
tendency  of  endocarditic  and  sclerotic  processes  to  attack  more 


EXAMINATION   OF   THE    CARDIOVASCULAR    SYSTEM          389 

than  one  valve,  either  simultaneously  or  consecutively.  When  they 
correspond  to  different  periods  of  the  cardiac  cycle,  it  is  compara- 
tively a  simple  matter  to  recognize  multiple  murmurs  by  their  different 
rhythms,  but  when  the  sounds  are  synchronous,  their  differentiation 
depends  upon  the  detection  of  separate  puncta  maxima  and  lines  of 
transmission,  and  upon  careful  study  of  individual  sound-quality 
and  other  tonal  attributes. 

The  basal  "see-saw"  bruit  of  aortic  obstruction  and  incompetence 
is  frequently  associated  with  the  apical  systolic  murmur  of  mitral 
leakage,  and  here,  aside  from  differences  in  tone,  rhythm,  and  maxi- 
mum intensities,  one  observes  three  distinct  lines  of  propagation — 
upward  into  the  neck  (aortic  systolic),  downward  over  the  sternum 
(aortic  diastolic),  and  toward  the  axilla  (mitral  systolic).  A  double 
lesion  at  the  mitral  orifice  produces  a  rough  presystolic  apical  rumble, 
continuous  with  a  softer  and  longer  systolic  murmur,  or  apparently 
separated  from  it  by  a  sharp,  snappy  cardiac  first  sound.  In  stenosis 
of  both  mitral  and  aortic  orifices  a  presystolic  apical  and  a  systolic  basal 
murmur  are  audible,  the  former  being  circumscribed  at  the  mitral 
area,  and  the  latter  conducted  upward.  In  the  combination  of 
mitral  stenosis  and  aortic  regurgitation  the  presystolic  apical  murmur 
of  the  former  defect  and  the  basal  diastolic  bruit  of  the  latter  some- 
times commingle  at  the  apex,  but  still  are  separable  by  their  slight 
differences  in  rhythm  and  by  their  decidedly  dissimilar  quality  and 
intensity.  Mitral  and  tricuspid  regurgitation  in  combination  create 
a  systolic  murmur  having  a  double  punctum  maximum,  that  of  the 
mitral  lesion  being  apical  and  that  of  the  tricuspid,  over  the  lower 
part  of  the  sternum;  between  these  two  intensity  points  there  lies  a 
spot  where  neither  murmur  is  distinct,  as  demonstrated  by  the  clear 
mitral  murmur  on  its  apical  side,  and  by  the  tricuspid  bruit  on  its 
sternal. 

Apart  from  differences  in  their  several  attributes,  multiple  murmurs 
must  be  discriminated  largely  by  associated  findings  relating  to 
structural  changes  in  the  cardiac  chambers,  to  the  peripheral  pulses, 
to  the  pulmonary  circulation,  and  to  sequels  such  as  edema,  cyanosis, 
and  dyspnea.  Auscultatory  findings  without  evidence  of  this  sort 
can  give  but  incomplete  data  regarding  the  character  of  a  murmurous 
lesion  and  its  effects  upon  the  cardiovascular  system. 

EXOCARDIAL  SOUNDS 

Pericardial  Friction. — Fibrinous  roughening  of  the  pericardial 
surfaces  generates  a  friction-sound  the  characteristics  of  which  are 
determined  by  the  amount  and  viscosity  of  the  exudate  and  by  the 


39° 


PHYSICAL    DIAGNOSIS 


force  of  the  cardiac  impact.  Ordinarily,  this  friction  is  most  dis- 
tinctly audible  along  the  left  sternal  border,  between  the  second  and 
fourth  interspaces  (Fig.  161);  less  commonly  it  is  most  intense  at 
or  near  the  apex  of  the  heart.  The  friction-sound  is  superficial, 
circumscribed,  and  usually  increased  by  moderate,  and  perhaps 
obliterated  by  very  forcible,  pressure  with  the  stethoscope;  it  is 
exaggerated  when  the  subject  bends  forward  in  the  upright  position, 
and  when  he  practises  Valsalva's  manoeuver  of  making  forced 
expiratory  efforts  while  the  glottis  is  closed.  The  rhythm  of  peri- 
cardial  friction  is  likely  to  be  to-and-fro,  corresponding  to  the  move- 
ments of  the  heart  rather  than  to  the  clinical  cardiac  tones  with 


Fig.   161. — Punctum  maximum  of  the  pericardial  friction-sound. 

which  it  is  not  exactly  synchronous;  rarely,  the  sound  is  tripled  by 
the  addition  of  a  presystolic  element  referable  to  auricular  systole. 
The  intensity  and  quality  of  a  pericardial  friction-sound  vary  greatly, 
according  to  the  pathologic  condition  existing  in  the  individual  case: 
when  greatly  roughened  and  very  dry  pericardial  surfaces  are  rubbed 
together  by  an  overacting  heart,  the  sounds  thereby  produced  are 
loud,  rasping,  grating,  or,  indeed,  not  unlike  the  creaking  of  leather; 
when  the  exudate  is  moist  and  buttery,  the  sounds  are  fainter,  and 
more  liquid  and  clicking  in  quality.  Pericardial  friction  is  a  curi- 
ously evanescent,  inconstant  sign,  in  that  it  may  be  detected  one  day 
and  be  absent  the  next,  and  may  change  its  punctum  maximum  from 


EXAMINATION   OF   THE    CARDIOVASCULAR   SYSTEM 


391 


time  to  time.  This  point  rises  as  an  effusion  collects,  and  should 
the  exudate  be  of  sufficient  volume  entirely  to  separate  the  two  layers 
of  the  pericardial  sac,  the  friction-sound  may  disappear,  reappearing 
later,  after  removal  or  resorption  of  the  fluid. 

An  endocardial  murmur,  in  comparison  with  pericardial  friction, 
is  a  softer,  less  superficial  sound,  accurately  corresponding  to  an 
event  of  the  cardiac  cycle,  and  having  a  fixed  punctum  maximum 
and  a  definite  line  of  transmission  or  area  of  localization;  furthermore, 
pressure  has  no  effect  whatever  upon  an  endocardial  bruit,  while 
Valsalva's  experiment,  as  a  rule,  enfeebles  it. 

Pleuropericardial  jriction,  though  acoustically  similar  to  a  peri- 
cardial rub,  bears  a.  definite  relation  to  the  cardiac  impulse  and  to 
the  respiratory  movements,  is  usually  most  intense  at  or  just  outside 
the  pulmonary  margin  bordering  on  the  triangle  of  cardiac  flatness, 
and  can  be  accurately  circumscribed  to  the  costal  pleura  or  to  the 
pericardial  reflection,  by  noting  the  effect  of  full  inspiration  and 
expiration  upon  the  sound.  (See  p.  168.) 

Cardiorespiratory  Murmurs. — When  a  segment  of  air-contain- 
ing lung  is  compressed  between  the  heart  and  the  chest-wall  the 
shock  of  the  cardiac  impulse  may  expel  the  air  from  the  compressed 
pulmonary  structure  with  sufficient  velocity  to  create  a  precordial 
murmur,  which  almost  invariably  is  of  systolic  rhythm.  Such  a 
sound  is  sometimes  audible  in  apparently  healthy  subjects,  especially 
in  those  whose  cardiac  action  is  tumultuous;  pathologically,  it  is 
detected  in  emphysema,  phthisis,  external  pericarditis,  and  massive 
pleural  effusion,  when  in  these  conditions  the  anterior  pulmonary 
margins  (particularly  the  lingula  of  the  left  lung)  are  crowded,  com- 
pressed, or  adherent  in  front  of  the  heart  so  as  to  receive  the  full 
force  of  the  cardiac  impact.  Ordinarily  a  cardiopulmonary  murmur 
resembles  a  short,  subdued  puff  or  whiff  of  air,  but  it  may  be  rela- 
tively prolonged,  loud,  and  rasping.  It  is  evanescent  in  charac- 
ter, restricted  to  a  limited  area,  intensified  by  deep  inspiration  and 
by  forward  inclination  of  the  trunk,  and  variously  modified  by 
cough  and  by  forced  respiration.  In  children  murmurs  of  this 
type  account  for  two-thirds  of  all  endocardial  adventitious  sounds. 

The  origin  of  diastolic  cardiopulmonary  murmurs  is  obscure,  and 
probably  the  mechanism  is  not  always  the  same.  In  some  in- 
stances rapid  aspiration  of  air  into  a  patch  of  lung  compressed  dur- 
ing ventricular  systole  (Potain)  serves  as  the  most  logical  explana- 
tion, while  hi  others  the  sound  is  best  explained  by  assuming  that 
adhesions  between  the  lung  and  the  heart  or  the  aorta  transmit 
a  local  suction  force  to  the  adherent  lung  at  the  period  of  cardiac 
diastole  (Gallavardin;  De  Vivo).  Should  the  portion  of  lung  shar- 


392  PHYSICAL   DIAGNOSIS 

ing  the  heart's  movements  be  the  seat  of  an  exudate  or  a  transu- 
date,  moist  cardiopneumatic  rales  also  may  be  appreciable.  (Cf. 
p.  166.) 

Pericardial  Succussion  Sounds. — The  presence  of  fluid  and  air 
within  the  pericardial  sac,  constituting  that  very  rare  clinical  entity 
hydropneumoperhardium,  gives  rise  to  a  melange  of  splashing, 
tinkling,  gurgling,  churning  sounds  audible  over  the  precordia,  and 
unmistakably  produced  by  the  movements  of  the  heart.  These 
sounds,  also  designated  as  the  metallic  gurgle  and  as  the  bruit  de 
nwulin,  are  sometimes  so  loud  as  to  be  appreciable  at  a  distance  from 
the  patient;  they  may  have  a  sharp  metallic  tone,  and  partly  or 
entirely  obscure  the  normal  cardiac  tones.  Pericardial  succussion 
sounds  must  be  distinguished  from  somewhat  similar  noises  created 
by  the  impact  of  the  heart  against  the  wall  of  an  adjacent  pulmonary 
cavity  containing  air  and  liquid,  or  against  a  left-sided  hydropneu- 
mothorax. 

VASCULAR   MURMURS 

Adventitious  sounds  may  be  heard  over  the  larger  arterial  and 
venous  trunks,  occasionally  in  health,  but  more  often  in  pathologic 
conditions.  Such  murmurs  are  explained  by  mural  vibrations,  by 
the  formation  of  intravascular  fluid  veins  due  to  a  local  anomaly  of 
the  vessel,  and  by  the  conduction  of  a  bruit  arising  at  a  crippled 
cardiac  orifice  or  within  an  aneurismal  sac.  Vascular  murmurs  may 
be  systolic,  diastolic,  or  to-and-fro;  continuous  or  intermittent;  and 
sighing,  humming,  musical,  or  harsh  in  quality,  according  to  the 
factors  of  their  production. 

Arterial  Murmurs. — If  one  of  the  larger  superficial  arteries 
(for  instance,  the  carotid)  be  auscultated,  the  transmitted  sounds  of 
the  heart  are  audible  as  dull,  muffled  systolic  and  diastolic  beats, 
but  if  pressure  with  a  stethoscope  be  made,  so  as  to  narrow  the  lumen 
of  the  vessel,  the  first  sound  becomes  louder  and  distinctly  murmurish, 
in  consequence  of  the  fluid  veins  formed  by  the  local  constriction 
(Fig.  162).  By  a  similar  mechanism  an  artery  constricted  by  adhe- 
sions, by  neoplasms,  or  by  enlarged  glands  is  also  the  seat  of  a  systolic 
bruit. 

A  systolic  murmur  over  the  carotids  is  a  confirmatory  sign  of  aortic 
stenosis  and  of  atheroma  or  aneurism  of  the  aortic  arch,  the  sound 
being  conducted  into  the  neck  from  its  site  of  origin  by  means  of  the 
blood-current.  A  systolic  murmur  over  the  subclavian  artery  is 
sometimes  audible  in  the  healthy  person,  when  the  breath  is  held 
with  the  lungs  fully  inflated;  and  in  apical  phthisis  a  similar  murmur 
may  occur  as  the  result  of  compression  of  the  subclavian  artery  by  a 


EXAM. NATION   OF   THE    CARDIOVASCULAR   SYSTEM 


393 


fibrous  band  of  adhesions.  This  subclavian  murmur  is  usually 
most  distinct  on  the  left  side,  in  the  outer  portion  of  the  infraclavicular 
space.  Systolic  carotid  and  subclavian  murmurs  sometimes  attend 


Fig.  162. — Mechanism  of  an  arterial  pressure  murmur. 

high-grade  anemias.     A  diastolic  murmur  over  the  carotids  and  the 
subclavians  is  generally  referable  to  the  conduction  of  a  bruit  generated 


Aneurism. 


Atheroma. 


Fig.  163. — Mechanism  of  arterial  murmurs  due  to  aneurism  and  to  atheroma. 


at  an  incompetent  aortic  orifice,  and  a  murmur  of  this  sort  is  audible 
without  the  slightest  compression  of  the  vessel  auscultated. 

Duroziez's  double  murmur  over  the  femoral  artery  is  audible  in 
many,  but  not  in  all,  cases  of  aortic  regurgitation.    When  the  examiner 


394  PHYSICAL   DIAGNOSIS 

listens  while  the  chest-piece  of  the  stethoscope  rests  very  lightly  upon 
the  vessel,  a  quiet  dull  systolic  thud  is  heard,  indicative  of  the  sudden 
impact  of  the  blood-column  against  the  arterial  wall;  with  moderate 
pressure  a  somewhat  harsh,  loud  murmur,  due  to  constriction  of  the 
vessel,  replaces  the  thud  first  detected;  and  with  still  greater  pressure, 
carefully  graduated  so  as  to  produce  just  the  proper  degree  of  arterial 
constriction,  the  soft  diastolic  murmur  of  arterial  reflux  becomes 
audible.  The  double  sound  (normal  systolic  pressure  murmur  and 
diastolic  reflux  bruit)  thus  developed  is  designated  as  Duroziez's 
sign. 

The  Venous  Hum. — This  sound,  also  known  as  the  bruit  de 
diable,  nun's  murmur,  and  humming-top  murmur,  is  heard  most 
distinctly  over  the  jugular  vein  at  the  inner  end  of  the  right  supra- 
clavicular  space,  whence,  if  the  sound  be  intense,  it  may  be  transmitted 
to  the  base  of  the  heart.  In  auscultation  of  the  jugulars  pressure 
upon  the  vessel  must  be  avoided,  for  a  fictitious  murmur  may  be 
excited  should  the  bell  of  the  stethoscope  compress  the  vessel  suffi- 
ciently to  constrict  it,  and  thus  to  produce  a  fluid  vein.  Exception- 
ally a  venous  hum  is  audible  over  the  courses  of  the  lateral  and 
longitudinal  sinuses,  over  the  liver,  and  over  the  subclavian  and 
axillary  veins. 

A  venous  hum  sounds  not  unlike  the  continuous  musical  soughing 
of  the  wind  through  bare  tree-tops,  or  the  aeolian-like  buzz  of  a 
mass  of  telegraph  wires  swept  by  a  breeze.  More  rarely  it  is  fitful, 
intermittent,  and  blowing  in  character.  The  murmur  has  a  rhythmic, 
crescendo  quality  during  forced  inspiration,  at  the  time  of  cardiac 
diastole,  and  when  the  patient  is  in  an  upright  position,  for  under 
these  circumstances  the  jugular  current  heartward  is  accelerated. 
It  is  intensified  when  the  patient  turns  the  head  sharply  away  from 
the  examiner,  thus  compressing  the  vein  and  narrowing  its  lumen. 
There  are  several  possible  factors  of  the  venous  hum,  none  of  which 
is  a  wholly  satisfactory  explanation  of  the  sign.  In  anemia  the 
hydremia  no  doubt  plays  a  part,  for  thin  blood  flows  with 
increased  rapidity  and  tends  to  form  whirling  jets;  but  a  more 
important  factor  in  this  condition  is  the  nutritional  relaxation  of 
the  walls  of  the  veins,  whereby  rapid  mural  vibrations  are  provoked. 
Chauveau's  theory  is  no  longer  seriously  entertained — that  in  anemic 
states  there  is  a  sort  of  compensatory  contraction  of  the  veins  because 
of  the  oligemia,  except  where  the  jugular  bulb  is  attached  to  the 
cervical  fascia,  at  which  point  a  relative  dilatation  exists,  and  here 
fluid  veins  are  formed.  Lorrain  Smith's  work  argues  a  decided 
increase  of  the  blood-mass  in  chlorosis,  and  no  great  diminution  of 


EXAMINATION   OF    THE    CARDIOVASCULAR    SYSTEM         395 

it  in  pernicious  anemia,  and  these  are  the  very  conditions  of  which 
venous  hums  are  most  frequently  symptomatic. 

The  venous  hum  is  not  necessarily  a  pathologic  sign,  since  it  is 
present  occasionally  in  perfectly  healthy  persons,  especially  in  the 
young.  It  usually  means  anemia,  however,  and  is  particularly 
suggestive  of  chlorosis  and  of  Addisonian  anemia.  No  definite 
relation  is  apparent  between  the  incidence  and  the  intensity  of  the 
sign  and  the  grade  of  the  blood  deterioration. 


SECTION  VI 
DISEASES  OF  THE  CARDIOVASCULAR  SYSTEM 


PERICARDITIS 

RHEUMATIC  fever  is  the  most  common  single  factor  of  pericarditis, 
although  it  is  difficult  to  determine  how  active  a  cause  it  is,  owing  to 
the  wide  divergence  in  the  percentages  (6  to  75)  given  by  different 
authorities;  averaging  these  data,  it  seems  safe  to  conclude  that  from 
30  to  40  per  cent,  of  all  cases  of  rheumatism  are  attended  by  peri- 
cardial  inflammation.  This  complication  is  prone  to  appear  during 
the  initial  attack  of  rheumatism,  and  bears  no  constant  relation  to 
the  number  or  intensity  of  the  articular  lesions,  though  it  appears  to 
be  especially  frequent  when  the  joints  of  the  upper  extremity  are 
attacked.  Nephritis,  gout,  diabetes,  and  the  hemorrhagic  diseases 
are  active  exciting  causes  of  pericarditis,  which  also  not  uncommonly 
attends  pneumonia  and  scarlatina,  and,  with  less  frequency,  other 
febrile  infections,  such  as  septicemia,  erysipelas,  variola,  diphtheria, 
measles,  and  enteric  fever.  A  pericardial  inflammation  may  be 
secondary  to  pleurisy,  bronchitis,  tonsillitis,  myocarditis,  or  valvular 
disease  of  the  heart  (especially  aortic  regurgitation) ,  or  it  may  develop 
in  consequence  of  some  neighboring  or  remote  septic  process — costal 
necrosis,  mediastinal  abscess  or  neoplasm,  empyema,  malignant  endo- 
carditis, gastric  or  esophageal  ulcer,  or  peritonitis.  Tuberculous 
pericarditis  occurs  both  in  a  primary  form  and  as  a  secondary 
process,  usually  in  connection  with  pleuropulmonary  tuberculosis. 
Chorea,  even  when  unaccompanied  by  arthritic  rheumatism,  is  not 
uncommonly  the  apparent  cause  of  a  pericardial  inflammation. 
Traumatic  pericarditis,  mainly  of  surgical  interest,  sometimes  super- 
venes in  consequence  of  a  penetrating  wound  of  the  heart  or  of  a 
violent  precordial  contusion. 

ACUTE  FIBRINOUS  PERICARDITIS  (Acute  Plastic  Pericarditis) 

Clinical  Pathology. — In  this  type  of  pericarditis  the  visceral 

and  parietal  layers  of  the  pericardium  are  covered,  universally  or  in 

patches,  with  a  fibrinous  exudate  attended  by  little  or  no  serous 

effusion,  the  underlying  serosa  being  dull,  swollen,  hyperemic,  and 

396 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  397 

often  ecchymotic.  In  recent  cases  of  mild  grade  the  fibrinous  exudate 
is  represented  by  a  delicate  pliable  membrane  of  yellowish-gray 
color  and  readily  detachable  from  the  underlying  serous  surface,  but 
in  older  lesions  the  deposit  is  thick,  tough,  and  firmly  adherent. 
Owing  to  the  movements  of  the  heart,  the  exudate  presents  a  ridged 
or  roughened  or  shaggy  appearance,  in  some  instances  matted  and 
meshed  like  two  buttered  surfaces  which  have  been  pressed  together 
and  then  separated,  while  in  other  instances  innumerable  shreds  of 
fibrin  attached  to  the  pericardium  produce  the  peculiar  shagginess 
distinctive  of  the  soTcalled  "hairy  heart,"  known  as  the  cor  hirsutum 
or  cor  villosum.  Myocardial  inflammation  occurs  in  severe  cases 
and  may  be  attended  by  dilatation,  but  in  mild  pericarditis  no  mus- 
cular changes  arise. 

Physical  Signs. — Inspection. — This  shows  nothing  characteristic, 
but  it  is  commonly  observed  that  the  apex-beat  is  rapid,  heaving,  and 
unnaturally  diffuse,  that  the  respirations  are  hurried  and  irregular, 
and  that  the  patient's  face  shows  anxiety  and  pain.  Diastolic 
pulsation  near  the  second  left  interspace  is  a  frequent  sign  in  in- 
cipient cases  (v.  i.). 

Palpation. — With  more  or  less  constancy  vibrations  produced  by 
the  to-and-fro  rub  of  the  roughened  pericardial  surfaces  are  felt, 
especially  toward  the  base  of  the  heart.  This  tactile  equivalent  of 
the  friction  sound  is  usually  more  intense  when  the  subject  is  erect 
than  when  dorsal  recumbency  is  assumed,  and  can  sometimes  be 
exaggerated  by  moderate,  and  obliterated  by  forcible,  pressure  with 
the  palm  of  the  hand.  Unlike  an  endocardial  thrill,  pericardial 
friction  fremitus  is  a  very  superficial  vibration,  does  not  exactly 
coincide  with  the  cardiac  beats,  and  has  a  peculiar  grating  quality 
quite  unlike  the  purring  vibrations  of  an  eddying  blood-stream. 
(See  p.  328.) 

Percussion. — In  so  far  as  it  relates  to  the  pericardial  inflammation, 
percussion  is  wholly  negative,  although  in  the  presence  of  cardiac 
dilatation,  which  may  develop  as  a  consequence,  a  corresponding 
extension  of  the  precordial  area  can  be  mapped  out. 

Auscultation. — The  pericardial  friction-sound  is  characteristic  of 
pericardial  inflammation,  if  three  other  potential,  though  rare, 
factors  of  such  a  sound  can  be  excluded:  excessive  dryness  and  vis- 
cosity of  the  pericardium,  as  in  Asiatic  cholera,  and  the  existence  of 
pericardial  ecchymoses  and  milk-spots.  Since  the  pericardial 
friction-sound  has  been  discussed  at  length  in  another  place  (p.  389), 
it  is  sufficient  here  to  note,  in  passing,  that  ordinarily  the  sign  is  most 
distinctly  heard  at  the  cardiac  base  and  along  the  left  sternal 
border;  that  it  has  a  double  rhythm  not  exactly  synchronous  with 


PHYSICAL   DIAGNOSIS 

that  of  the  heart;  that  it  resembles  a  surface  sound,  more  or  less 
influenced  by  local  pressure  and  by  the  force  of  the  cardiac  impact ; 
and  that  its  quality  ranges  between  that  of  a  soft  papery  rustle  and 
that  of  rude  parchment-like  grating  or  even  of  creaking  leather — 
bruit  de  cuir  neuf. 

Diagnosis. — The  friction-sound,  precordial  pain,  and  moderate 
fever  are  the  three  physical  signs  pointing  to  acute  plastic  pericar- 
ditis. An  intense  clanging  accentuation  of  the  pulmonic  second 
sound  (Turrettini's  eclat  clangoreaux  diastolique)  accompanies,  if 
not  precedes,  the  friction-sound  in  many  instances,  especially  those 
in  which  the  infection  is  circulatory  rather  than  by  extension  from  a 
pleuritis.  The  pleuropericardial  friction-sound  of  pleurisy  differs 
from  a  true  pericardial  rub  hi  being  most  intense  along  the  left  edge 
of  the  heart,  and  in  having  the  characteristics  of  a  cardiopulmonary 
sound  which  is  definitely  affected  by  the  different  respiratory  phases 
in  the  manner  elsewhere  explained.  (See  p.  168.)  In  differen- 
tiating a  murmur  of  endocarditis  the  punctum  maximum,  area  of 
transmission,  pulse  peculiarities,  cardiac  tonal  changes,  and  at- 
tendant myocardial  alterations  are  the  dependable  criteria.  (See 
P-  374-) 

SEROFIBRINOUS  PERICARDITIS  (Serous  Pericardial  Effusion) 

Clinical  Pathology. — In  this  type  an  initial  stage  of  dry  serositis 
is  soon  succeeded  by  the  escape  of  an  abundant  serofibrinous  effusion 
from  the  engorged  capillaries,  the  serum  thus  poured  out  collecting 
within  the  pericardial  sac  and  the  fibrin  being  deposited  upon  the 
serous  surfaces  in  the  form  of  a  coating  of  variable  thickness  and 
distribution.  The  effusion  may  be  virtually  a  clear  serous  fluid, 
but,  as  a  rule,  it  is  more  or  less  opaque  from  the  presence  of 
fibrin-flakes  and  leukocytes,  while  in  conditions  of  cachexia,  in 
tuberculosis,  and  in  malignant  disease  the  liquid  is  not  unlikely  to  be 
blood  stained.  The  volume  of  the  effusion  may  range  from  a  few 
ounces  to  10  (300  cc.)  or  more;  exceptionally,  as  in  the  case  of  gradu- 
ally accumulating  effusions,  it  amounts  to,  or  even  exceeds,  a  quart 
(1000  cc.).  Chemically  and  microscopically,  a  pericardial  exudate 
does  not  differ  materially  from  inflammatory  fluids  derived  from  other 
serous  membranes.  (See  p.  53.)  Complete  absorption  of  an  effusion 
containing  little  or  no  fibrin  may  leave  the  pericardial  serosa  practically 
unimpaired,  but  as  a  rule  sufficient  plastic  material  remains  after  the 
absorption  of  the  serous  exudate  to  cause  a  variable  degree  of  fibrous 
union  between  the  opposed  serous  layers.  Local  deposits  of  organized 
fibrin  are  recognized  as  milk-spots  or  indurated  white  opaque  areas 
on  the  visceral  pericardium.  The  myocardium  shows  degenerative 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM  399 

or  inflammatory  changes,  and  endocarditis  commonly  coexists, 
usually  in  consequence  of  the  same  factor  responsible  for  the  peri- 
carditis, but  exceptionally  arising  by  extension  of  the  serosal  in- 
flammation through  the  myocardium. 

Physical  Signs. — Inspection. — In  the  young  child  a  large  effusion 
causes  unnatural  prominence  of  the  precordia,  but  the  more  rigid 
chest-wall  of  the  adult  does  not  perceptibly  bulge  in  this  manner. 
The  apex-beat,  if  not  wholly  obscured  by  the  effusion,  is  visibly 
enfeebled  and  displaced  from  its  accustomed  site.  Ordinarily, 
there  is  pulsation  an  interspace  or  two  above  the  normal  apical 
area,1  though  sometimes  the  apex-beat  is  lowered,  owing  to  depression 
of  the  diaphragm  by  a  copious,  heavy  exudate  within  the  pericardial 
sac.  In  this  event  there  may  be  also  a  local  epigastric  prominence 
(Auenbrugger's  sign),  due  to  descent  of  the  left  lobe  of  the  liver. 
Ewart's  sign,  or  prominence  of  the  sternal  end  of  the  left  first  rib 
with  elevation  of  the  head  of  the  clavicle,  is  a  finding  of  some  sugges- 
tiveness.  Other  associated  signs,  of  variable  constancy,  include  re- 
striction or  abolition  of  the  diaphragm  shadow,  left  unilateral  diminu- 
tion of  expansion,  and  rapid,  difficult  breathing,  sometimes  amounting 
to  orthopnea.  There  may  be  cyanosis  or  chalky  pallor,  engorgement 
of  the  veins  of  the  neck,  and  pressure  phenomena,  such  as  extreme 
precordial  oppression  and  pain,  distressing  cough,  dysphagia,  hoarse- 
ness, and  even  aphonia. 

The  detection  by  the  fluoroscope  of  the  normal  inspiratory  clear 
zone  between  the  diaphragm  and  the  cardiac  apex  is  proof  positive 
of  no  fluid  in  the  pericardial  sac.  Little  or  no  transmission  of  ven- 
tricular pulsation  to  the  air  bubble  in  the  stomach  is  a  rontgeno- 
scopic  sign  upon  which  Maragliano  lays  stress  in  the  diagnosis  of  an 
intervening  mass  of  pericardial  fluid. 

Palpation. — The  palpating  hand  confirms  the  findings  noted  by 
visual  examination,  particularly  those  relating  to  precordial  fulness, 
the  apical  impulse,  the  respiratory  embarrassment,  and  the  altered 
anatomic  relations  on  the  left  side.  In  some  instances  basal  friction 
.  is  palpable,  despite  the  accumulation  of  considerable  fluid  in  the 
pericardial  sac. 

The  pulse  is  usually  found  to  be  of  increased  frequency,  low 
tension,  and  disordered  rhythm.  Though  by  no  means  pathog- 

1  To  all  intents  and  purposes  this  represents  the  apex  beat,  though,  as  Ewart 
insists,  there  is  good  reason,  in  some  instances,  to  attribute  the  impulse  to  the 
impact  of  the  body  of  the  right  ventricle.  Cal vert's  recent  researches  show 
that  the  position  of  the  heart  depends  chiefly  upon  its  size,  the  apex  remaining 
in  the  normal  position  so  long  as  compensation  is  preserved  and  the  size  of  the 
heart  is  unaltered,  but  being  displaced  backward  and  toward  the  right  when, 
with  failing  compensation,  the  heart  becomes  unduly  small  by  fault  of  a  dimin- 
ished blood-supply. 


400  PHYSICAL    DIAGNOSIS 

nomonic,  the  pulsus  paradoxus,  which  dies  out  at  the  end  of 
inspiration,  is  a  sign  of  some  corroborative  value  in  the  diagnosis 
of  a  large  effusion.  (See  p.  338.) 

Percussion. — Percussion  reveals  an  unnaturally  large  area  of 
cardiac  flatness,  which  in  a  bulky  effusion  may  conform  to  the 
outline  of  a  pyramid  having  its  base  downward  and  its  apex  in  the 
upper  sternal  region.  Diminution  in  the  size  and  alteration  in  the 
shape  of  this  area  of  flatness  are  occasionally  demonstrable  when 
the  subject  changes  from  an  erect  posture  to  dorsal  decubitus.  The 
normal  acuteness  of  the  cardiohepatic  angle  is  made  obtuse  by  the 
sagging  of  the  pericardial  sac,  and  flatness  is  substituted  for  the 
resonance  normally  found  in  the  fifth  right  interspace  at  the  sternal 
border — Rotch's  sign.  An  effusion  of  too  moderate  a  size  to  produce 
well-defined  precordial  flatness  will  afford  this  suggestive  area 
of  flatness  in  the  space  between  the  borders  of  the  heart  and  the 
liver.  (See  Fig.  134.)  The  upper  inner  angle  of  Traube's  space 
may  be  encroached  upon  by  an  effusion  of  large  volume.  It  may 
be  possible  to  delimit  an  obtuse  angle  formed  at  the  level  of  the 
third  costal  cartilage  by  the  normal  area  of  supracardiac  vascular 
dulness  and  the  left  border  of  pericardial  flatness — Sibson's  notch. 
Compression  of  the  lower  lobe  of  the  left  lung  by  an  effusion  of 
large  volume  may  produce,  in  the  left  infrascapular  region,  a  small 
patch  of  dulness  over  which  increased  vocal  fremitus,  bronchophony, 
and  bronchial  breathing  are  detected  when  the  patient  sits  erect,  but 
not  when  he  leans  forward,  lies  in  right  lateral  decubitus,  or  assumes 
the  knee-chest  posture  (Bamberger;  Pin);  or  there  may  be  dulness, 
with  abolished  voice  and  respiratory  sounds,  at  the  base  of  the  left 
lung  alongside  the  spine  (Ewart) .  In  certain  instances  a  circum- 
scribed patch  of  bronchial  breathing  is  audible  in  the  right  mammary 
region  below  the  nipple.  Compression  of  the  left  lung  by  a  large 
effusion  may  account  for  a  midaxillary  area  of  dulness  or  of  skodaic 
resonance,  over  which  the  voice  and  breath-sounds  are  either  sup- 
pressed or  greatly  exaggerated,  and  this  group  of  signs  also  is  de- 
cidedly affected  by  postural  changes. 

Auscultation. — The  cardiac  sounds  are  indistinct,  muffled,  or 
inaudible,  except  at  the  base,  where  increased  intensity  of  the  second 
sound  is  the  rule.  Here  also  friction-sounds  are  prone  to  persist, 
in  contrast  to  the  auscultatory  silence  over  the  precordia  below  this 
level.  With  absorption  of  the  exudate,  however,  a  corresponding 
increase  in  the  extent  of  the  friction  area  is  to  be  expected,  with 
reappearance  of  the  cardiac-sounds.  The  various  modifications  of 
the  respiratory  sounds  audible  over  patches  of  compression  atelectasis 
have  been  mentioned  in  the  preceding  paragraph. 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  401 

Diagnosis. — Displacement  and  enfeeblement  of  the  apex-beat, 
an  enlarged  precordial  area  of  pyramidal  outline,  flatness  in  the 
cardiohepatic  angle,  muffling  of  the  heart-sounds,  and  evidences  of 
pulmonary  compression  are  the  principal  diagnostic  signs  of  an 
effusion  in  the  pericardial  sac. 

In  differentiating  cardiac  dilatation  it  is  helpful  to  remember  that 
the  apex-beat  of  a  dilated  heart  marks  the  extreme  lower  and  outer 
limit  of  the  cardiac  outline,  and  does  not  lie  well  within  this  boundary, 
as  it  does  in  a  pericardial  effusion;  and  that  the  flatness  of  a  dilated 
heart,  though  exceptionally  pyramidal,  is  generally  of  ovoid  shape, 
does  not  extend  so  high  as  the  flatness  of  an  effusion,  and  shades  off 
gradually  into  the  surrounding  pulmonary  resonance,  so  that  no 
sharp  line  of  demarcation  between  the  two  is  appreciable,  as  is 
usually  the  case  with  effusion  flatness.  A  history  of  chronic  valvular 
disease  or  of  myocarditis  suggests  dilatation,  just  as  a  story  of  rheu- 
matic fever  and  acute  plastic  pericarditis  is  in  favor  of  effusion. 
Neither  the  character  of  the  apical  impulse  nor  the  effect  of  postural 
changes  on  the  area  of  cardiac  flatness  is  a  reliable  differential  point; 
and  the  cardiohepatic  angle  may  be  dulled  by  a  dilated  right  ventricle. 

A  left  pleural  effusion,  especially  when  encapsulated  near  the 
heart,  may  suggest  a  pericardial  effusion  of  large  volume,  but  ordi- 
narily a  confusion  of  this  sort  is  disposed  of  without  difficulty.  Pleu- 
risy is  indicated  by  the  history  of  an  acute  stitch  in  the  side,  a  pleural 
friction-sound,  Grocco's  sign,  flatness  over  the  anterolateral  and 
generally  the  posterior  regions  of  the  thorax,  and  by  the  failure  to 
discover  such  important  pericarditic  signs  as  basal  friction,  extension 
of  precordial  flatness,  and  enfeeblement  of  the  cardiac  tones.  In 
the  event  of  a  puzzling  group  of  physical  signs,  as  in  the  case  of 
coexisting  pericardial  and  pleural  effusion,  the  #-ray  may  settle  the 
diagnosis  beyond  all  question. 

Exceptionally,  enlargement  of  the  area  of  cardiac  flatness  is 
referable  to  pulmonary  retraction,  to  aortic  aneurism,  or  to  mediastinal 
neoplasm,  but  none  of  these  conditions  creates  pyramid-shaped 
flatness,  and  each  of  them  is  attended  by  physical  signs  and  by  a 
clinical  history  that,  if  intelligently  reviewed,  are  sufficient  for 
differentiation. 

PURULENT    PERICARDITIS    (Pyopericardium  j    Empyema   of  the  Pericardium; 
Pericardial  Abscess) 

Clinical  Pathology. — This  most  grave  variety  of  pericarditis, 
characterized  by  an  effusion  of  pus  within  the  pericardial  sac,  is  more 
frequent  in  children  than  in  adults,  and  generally  is  traceable  to 

26 


402  PHYSICAL    DIAGNOSIS 

pyemia,  to  some  neighboring  local  purulent  focus,  or  to  an  acute 
specific  infectious  process  like  pneumonia  or  tuberculosis.  The 
exudate  varies  in  character  according  to  conditions  prevailing  in  the 
individual  case,  being  in  some  a  thin  limpid  liquid  and  in  others  a 
collection  of  creamy  material  containing  a  minimal  amount  of  serum 
and  fibrin  and  composed  chiefly  of  pus  cells,  the  extraordinary  number 
of  which  constitutes  the  striking  difference  between  this  and  the 
ordinary  serofibrinous  type  of  effusion.  The  pus  is  but  rarely 
•  absorbed  spontaneously,  although  sometimes  the  more  liquid  portions 
are  thus  disposed  of,  leaving  an  amorphous  mass  of  caseous  matter 
tending  ultimately  to  undergo  calcification.  Instrumental  evacuation 
of  the  pus  results  in  permanent  adhesion  of  a  variable  area  of  the 
two  pericardial  layers,  already  unduly  thickened  and  granular  from 
the  intense  purulent  inflammation  by  which  they  have  been  attacked. 
Spontaneous  evacuation  of  a  pericardial  abscess,  as,  for  example, 
by  its  discharge  through  the  chest  wall  or  into  the  mediastinal  cavity, 
is  a  possible,  but  very  remote,  sequel,  should  the  patient  live.  It  is 
obvious  that  the  myocardial  changes  in  purulent  pericardial  effusions 
must  be  of  greater  intensity  than  those  attending  simple  serofibrinous 
exudates,  and  in  some  instances  purulent  infiltration  of  the  heart 
muscle  takes  place. 

Physical  Signs. — The  aspirating  needle  is  the  only  certain  means 
of  distinguishing  a  purulent  from  a  serofibrinous  pericardial  effusion 
whose  local  subjective  signs  are  practically  identical.  On  academic 
grounds  it  is  sometimes  taught  that  extreme  precordial  bulging  and 
hepatic  displacement,  with  local  edema  or  even  discoloration,  mean 
pus  in  the  pericardial  sac,  but,  clinically,  this  dramatic  symptom- 
group  virtually  never  appears.  It  is  not  unusual,  however,  to  find 
great  prostration,  rapid  emaciation,  recurrent  rigors,  widely  fluctua- 
ting fever,  leukocytosis,  and  iodophilia  in  purulent  cases,  together 
with  a  history  of  some  cause  capable  of  setting  up  a  purulent  inflamma- 
tion. But  inasmuch  as  the  foregoing  evidence  is  more  often  equivocal 
than  definite,  pericardicentesis,  in  the  vast  majority  of  cases,  is  the 
key  to  the  situation.  (See  p.  54.) 

CHRONIC    ADHESIVE    PERICARDITIS    (Adherent    Pericardium;    Mediastino- 

pericarditis) 

Clinical  Pathology. — Pericardial  adhesions,  formed  by  the 
organization  of  inflammatory  material,  ordinarily  are  the  relic  of  a 
well-defined  attack  of  acute  pericarditis,  but  in  some  instances  the 
fibrosis  arises  insidiously,  with  no  authentic  history  of  a  primary 
inflammation.  In  either  event  the  process  is  essentially  of  a  chronic 


DISEASES    OP    THE    CARDIOVASCULAR   SYSTEM          •  403 

nature,  and,  in  accordance  with  its  anatomic  distribution,  is  separable 
into  two  principal  groups,  the  internal  and  the  external,  which  types, 
it  is  to  be  remembered,  are  frequently  combined.  Internal  pericardial 
adhesions,  confined  to  the  pericardial  sac,  commonly  exist  as  scattered 
fibrous  strands  or  filaments  connecting  the  parietal  and  visceral 
layers  of  the  pericardium,  which  also  is  generally  the  seat  of  con- 
siderable thickening  and  induration.  These  strands  vary  in  length 
according  to  their  situation,  being  longest  near  the  apex  of  the  heart, 
where  the  cardiac  excursions  exert  the  greatest  traction,  and,  as  the 
result  of  this  strain,  a  filament  may  be  torn  from  one  of  its  attachments, 
so  that  it  dangles  free  in  the  pericardial  cavity.  In  some  cases  the 
adhesions  are  represented  merely  by  a  few  patches  of  simple  union 
between  the  two  membranes,  and  in  others  a  moderate  fibrosis  of 
the  pericardium,  rather  than  actual  adhesions,  is  the  predominant 
lesion,  conditions  such  as  these  often  being  quite  symptomless  and 
leading  to  no  damage  to  the  myocardium.  In  contrast  to  these 
relatively  benign  local  processes,  it  occasionally  happens  that  the 
parietal  and  visceral  pericardium  are  universally  adherent,  thickened, 
and  tightly  welded  into  a  single  structure,  the  normal  pericardial  sac 
being,  in  consequence,  entirely  obliterated,  and  to  this  condition 
the  term  adherent  pericardium  is  applicable.  Investment  of  the 
heart  by  an  unyielding  bony  capsule  supervenes  when  an  adherent 
pericardium  undergoes  calcification,  as  is  the  case  in  exceptional 
examples  of  this  type  of  fibrosis.  In  early  life  the  incessant  com- 
pression exerted  by  a  dense  and  firmly  contracting  adherent  peri- 
cardium is  capable  of  causing  actual  atrophy  of  the  heart.  External 
pericardial  adhesions,  almost  always  attended  by  internal  union  of 
the  layers,  may  anchor  the  outer  surface  of  the  pericardium  to  the 
adjacent  chest-wall,  the  pleura,  the  diaphragm,  and  the  mediastinal 
structures — a  most  serious  condition  of  indurative  mediastinoperi- 
carditis  (q.  v.~),  tending  to  cause  great  hypertrophy  and  dilatation 
of  the  heart,  advanced  myocardial  degeneration,  and  sometimes 
to  provoke  inflammatory  implication  of  the  subphrenic  structures. 
The  cardiac  enlargement  commonly  but  by  no  means  invariably 
met  with  in  the  different  types  of  chronic  adhesive  pericarditis, 
especially  when  external  adhesions  exist,  is  attributable  to  several 
factors:  hypertrophy  and  subsequent  dilatation  may  be  due  to  mechan- 
ical interference  with  the  movements  of  the  heart,  to  compression 
stenosis  of  large  arterial  trunks,  or  to  associated  valvular  defects, 
while  pure  dilatation  is  frequently  set  up  by  the  coexisting  myo- 
carditis. The  right  ventricle,  being  relatively  weak,  thin-walled, 
and  predisposed  anatomically  to  external  adhesions,  is  likely  to  be 


4°4  PHYSICAL   DIAGNOSIS 

damaged  more  seriously  by  these  structural  changes  than  the  left 
ventricle. 

Physical  Signs. — Inspection. — Visual  examination  may  discover 
practically  all  the  important  evidences  of  chronic  adhesive  peri- 
carditis, or  those  referable  to  fixation  of  the  heart  to  neighboring 
structures  and  to  the  direct  tug  upon  different  parts  of  the  chest-wall 
produced  by  the  contractions  of  the  adherent  organ.  There  may 
be  no  physical  signs  whatever  of  adherent  pericardium,  in  the  absence 
of  adhesions  between  the  external  layer  of  the  sac  and  the  thoracic 
wall,  diaphragm,  and  pleura.  In  the  presence  of  extensive  adhesions 
there  is  fixation  of  the  apex-beat,  which  being  restricted  and  bound 
down  by  fibrous  tissue,  cannot  gravitate  toward  the  dependent  side 
when  the  subject  changes  from  left  to  right  lateral  decubitus  or  vice 
versa,  nor  can  it  descend  at  the  close  of  a  full  inspiration.  Systolic 
retraction  of  a  small  area  of  the  thoracic  surface  in  the  neighborhood 
of  the  apex  is  also  noted;  rarely  a  similar  recession  of  several  inter- 
spaces and  their  corresponding  costal  cartilages  to  the  left  of  the 
sternum,  and  even  retraction  of  the  lower  part  of  this  bone  are 
perceived.  Sometimes  there  is  a  decidedly  undulatory  precordial 
impulse — Sander's  sign.  J.  F.  H.  Broadbent  has  described,  as  a 
pathognomonic  sign  of  extensive  pericardial  adhesions,  systolic 
retraction  of  the  tenth  and  eleventh  intercostal  spaces  in  the  left 
infrascapular  region,  and  also,  less  commonly,  of  the  seventh  and 
eighth  interspaces  anteriorly — Broadbent' s  sign.  (See  p.  324.) 
Under  the  same  circumstance  Sir  William  H.  Broadbent  has  noted 
that  the  normal  epigastric  movements  during  respiration  are  greatly 
hampered,  if  not  quite  abolished.  Friedreich's  sign  (diastolic  collapse 
of  the  jugular  veins)  and  Kussmaul's  sign  (inspiratory  jugular  turges- 
cence)  are  inconstant  findings,  in  no  wise  distinctive  of  adhesive 
pericarditis.  (See  p.  326.)  As  the  right  ventricle  fails,  dyspnea 
becomes  distressing,  cyanosis  appears,  and  edema  and  other  forms 
of  dropsy  develop.  Anasarca  and  effusions  into  the  peritoneum 
and  the  pleura  have  been  observed  as  the  effect  of  pressure  upon 
the  large  azygos  vein  (J.  Lloyd  Roberts). 

Palpation. — Exceptionally,  a  diastolic  shock  is  felt  over  areas  that 
show  systolic  retraction,  and  this  sign,  due  to  the  sudden  rebound  of 
the  chest-wall  directly  after  systole,  is  regarded  as  diagnostic. 
As  in  pericardiul  effusion,  the  pulse  in  adhesive  pericarditis  not 
uncommonly  conforms  to  the  paradoxic  type.  The  fixed  position 
of  the  apex-beat  is  clearly  appreciated  by  palpation. 

Percussion. — The  area  of  cardiac  flatness  may  be  increased, 
commonly  in  all  directions,  the  increase  being  referable  both  to  the 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  405 

enlargement  of  the  heart  and  to  fibrosis  and  retraction  of  the  anterior 
margins  of  the  lung.  If  the  latter  be  anchored  by  pleuropericardial 
adhesions,  comparative  percussion  will  fail  to  show  the  diminution 
of  cardiac  flatness  which  occurs  normally  at  the  end  of  a  full  inspira- 
tion. D  ulness  in  the  cardiohepatic  angle  has  been  found  in  adhesive 
pericarditis,  as  well  as  in  pericardial  effusion  (q.  v.  s.). 

Auscultation. — There  are  no  definite  auscultatory  evidences  of 
true  adherent  pericardium,  but  in  mediastinopericarditis  there  may 
be  a  peculiar  creaking  friction-sound  audible  over  the  sternum  dur- 
ing up-and-down  movements  of  the  subject's  arms  (Perez;  Bab- 
cock).  (See  p.  168.)  A  pericarditic  friction-sound,  not  unlike  the 
presystolic  rumble  of  mitral  stenosis  (q.  v.} ,  is  present  in  some  cases, 
but  not  with  any  degree  of  constancy.  In  the  presence  of  exten- 
sive adhesions  pleuropericardial  friction-sounds  are  commonly 
heard  over  the  anterior  pulmonary  borders  surrounding  the  body 
of  the  heart.  The  cardiac  sounds  are  those  of  hypertrophy  or  of 
dilatation,  according  to  which  condition  predominates. 

Diagnosis. — Fixation  of  the  apex-beat,  immobility  of  the  anterior 
pulmonary  borders,  systolic  retraction  and  diastolic  shock,  cardiac 
enlargement,  pericarditic  friction,  paradoxic  pulse  changes,  and 
phenomena  relating  to  the  jugular  veins  form  a  combination  of  signs 
that  unmistakably  indicates  chronic  pericarditis  with  extrapericar- 
dial  adhesions,  and  in  such  cases  a  history  of  previous  pericarditis  is 
usually  obtainable,  to  make  the  diagnosis  doubly  certain.  As 
noted  above,  simple  internal  adhesion  of  the  two  pericardial  layers 
is  essentially  a  latent  process,  giving  rise  to  no  distinctive  symptoms 
nor  physical  signs.  In  doubtful  cases — and  these  are  numerous — 
one  can  venture  only  a  provisional  diagnosis,  based  upon  a  history 
of  pericardial  inflammation,  and  upon  a  clinical  picture  of  chronic 
circulatory  failure,  respiratory  distress,  right  ventricular  dilatation, 
and,  sometimes,  friction-sounds  over  the  precordia. 

Pericarditic  hepatic  pseudocirrhosis,  associated  with  ascites  and 
with  a  hard,  contracted  liver,  counterfeits  ordinary  alcoholic  cirrho- 
sis of  this  organ,  especially  in  those  cases  in  which  the  cardiac  phe- 
nomena are  latent  or  overshadowed  by  those  of  portal  obstruction. 
In  this  differentiation,  apart  from  the  cardiac  signs,  Laennec's 
cirrhosis  is  suggested  by  a  history  of  alcoholism  or  of  syphilis,  by  a 
symptomatology  characterized  by  long-standing  gastro-intestinal 
catarrh,  hematemesis,  melena,  and  hemorrhoids,  and  by  the  appear- 
ance of  ascites  followed  by  edema  of  other  parts.  In  contrast,  Pick's 
pseudocirrhosis  is  indicated  by  a  history  of  rheumatism,  by  symptoms 
referred  to  the  heart,  and  by  the  onset  of  edema  of  dependent  parts 
prior  to  the  development  of  ascites. 


4C>6  PHYSICAL    DIAGNOSIS 


HYDROPERICARDIUM    (Pericardial   Dropsy) 

Hydropericardium  is  usually  part  of  general  dropsy,  cardiac  or 
renal,  but  it  may  arise  in  consequence  of  the  pressure  of  an  aneurism 
or  of  a  mediastinal  neoplasm.  Under  exceptional  circumstances 
the  fluid,  instead  of  being  a  clear  serum,  is  milky  from  the  presence 
of  chyle — chylopericardium.  The  transudate  seldom  attracts  atten- 
tion, for,  being  non-inflammatory  and  of  moderate  volume,  it  does 
not  readily  to  provoke  conspicuous  objective  symptoms.  Physical 
signs,  when  present,  include  moderate  dyspnea  and  perhaps  pre- 
cordial  uneasiness,  with  the  flatness  of  a  liquid  pericardial  effusion 
which  most  readily  shifts  with  changes  of  posture,  and  which  is 
unaccompanied  by  friction,  fever,  pain,  or  precordial  prominence. 
These  peculiarities  plus  a  story  of  cardiorenal  disease  and  the  dis- 
covery of  subcutaneous  dropsy  or  of  hydrothorax,  serve  to  differen- 
tiate hydropericardium  from  a  pericarditic  effusion. 

HEMOPERICARDIUM    (Pericardial   Hemorrhage) 

Hemopericardium,  or  free  hemorrhage  into  the  pericardial  sac, 
is  a  rare  and  rapidly  fatal  accident,  and  one  to  be  clearly  distin- 
guished from  the  hemorrhagic  pericarditic  effusions  sometimes 
met  with  in  tuberculous,  cancerous,  and  cachectic  subjects  (see  p.  398) . 
Ordinarily  hemopericardium  is  due  to  the  bursting  of  aneurism 
springing  from  the  intrapericardial  portion  of  the  aorta  or  from  a 
coronary  artery;  exceptionally  the  blood  pours  out  from  a  chamber 
of  the  heart  ruptured  by  fault  of  advanced  myocardial  destruction; 
and  sometimes  the  hemorrhage  follows  a  wound  of  the  heart.  In 
any  event  the  physical  signs  are  those  of  effusion,  and  are  attended 
(as  well  as  overshadowed)  by  acute  dyspnea,  precordial  pain, 
shock,  and  circulatory  failure. 

t 

PNEUMOPERICARDIUM      (Pyopneumopericardiom;     Hydropneumo- 
pericardium;    Hemopneumopericardium  ! 

Pneumopericardium,  or  the  presence  of  gas  within  the  pericardial 
sac,  is  almost  invariably  associated  with  a  liquid  effusion,  usually 
purulent  (pyopneumoperkardium) ,  sometimes  serous  (hydropneu- 
mopericardiuni) ,  and  exceptionally  hemorrhagic  (liemopneumo- 
perkardium).  The  affection  usually  depends  upon  the  entrance 
of  air  through  a  traumatic  breach  or  by  way  of  a  fistulous  tract 
leading  from  a  neighboring  organ,  but  the  pericardium  may  fill  with 
gas  generated  by  the  decomposition  of  an  exudate  therein.  Owing 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  407 

to  the  practical  constancy  of  bacterial  contamination,  purulent 
pericarditis  is  a  very  frequent  complication.  The  direct  effect  of 
pneumopericardium  is  distention  of  the  pericardial  cavity  with  gas 
and  with  liquid,  the  former  occupying  the  upper,  and  the  latter 
filling  the  lower,  part  of  the  space.  This  distention,  if  decided,  leads 
to  embarrassment  of  the  cardiac  action  and  to  displacements  of 
the  heart,  lungs,  and  diaphragm  similar  to  those  met  with  in  ordi- 
nary liquid  pericardial  effusions. 

The  physical  signs  vary  with  the  degree  of  pericardial  distention 
and  with  the  character  and  the  volume  of  the  exudate.  The  pre- 
cordial  interspaces  are  leveled  or  bulged  and  the  precordia  itself 
may  be  unnaturally  prominent;  the  apex-beat  is  obscure,  if  not 
wholly  effaced,  but  it  may  become  both  visible  and  palpable  when 
the  subject  leans  forward  so  as  to  bring  the  heart  closer  to  the  parietes. 
There  is  tympany  (perhaps  with  a  metallic  or  a  cracked-pot  tone) 
over  the  upper  part  of  the  cardiac  area,  with  flatness  below,  as  the 
liquid  effusion  accumulates,  the  relative  positions  of  these  two  areas 
being  modified  by  postural  changes.  Auscultation,  which  affords 
most  distinctive  signs,  reveals  more  or  less  pericardial  friction  inter- 
mingled with  a  medley  of  churning,  splashing,  tinkling  sounds, 
among  which  can  be  distinguished  the  hard  tone  of  the  metallic 
gurgle  and  the  liquid  purl  of  the  bruit  de  moulin  (see  p.  392).  These 
adventitious  sounds,  synchronous  with  the  movements  of  the  heart, 
may  effectually  mask  the  cardiac  tones,  and  the  rising  pericardial 
exudate  has  a  similar  effect.  Extreme  pneumopericardial  distention 
is  likely  to  cause  great  dyspnea,  cyanosis,  severe  precordial  oppres- 
sion and  pain,  distressing  palpitation,  syncopal  attacks,  and  a  small, 
erratic  pulse;  but  in  less  urgent  cases  the  picture  is  very  like  that  of 
pericarditis. 

Pneumopericardium  must  be  distinguished  from  left  pneumo- 
thorax  and  from  gaseous  distention  oj  the  stomach,  the  differentiating 
points  in  the  first  instance  being  a  displaced  and  pulsating  cardiac 
area  associated  with  metallic  and  splashing  sounds  of  palpably 
respiratory  origin,  and  in  the  second  instance  the  disappearance  of 
similar  adventitious  sounds  immediately  after  the  passage  of  a 
stomach-tube  to  remove  the  gas. 

CARDIAC  HYPERTROPHY 

Clinical  Pathology. — An  adequately  nourished  heart  subjected 
to  habitually  increased  work  in  time  undergoes  hypertrophy,  or  an 
increase  in  its  muscular  structure,  this  enlargement  being  designated 


408 


PHYSICAL   DIAGNOSIS 


as  general  or  as  partial,  according  to  its  distribution.  Not  infre- 
quently a  single  chamber  is  affected,  or  the  change  may  be  restricted 
to  one  entire  side  or  to  a  chamber  on  each  side,  while  a  still  sharper 
limitation  of  the  hypertrophy  to  a  small  local  area  of  the  heart  is 
termed  circumscribed.  Pathologically,  two  well-defined  types  of 
cardiac  hypertrophy  are  recognized:  simple  hypertrophy,  or  thickening 
of  the  cardiac  wall  with  no  deviation  from  normal  in  the  size  of  the 
corresponding  chamber;  and,  eccentric  hypertrophy,  in  reality  hyper- 
trophy with  dilatation,  characterized  by  thickening  of  the  wall  with 
enlargement  of  the  chamber.  So-called  "concentric  hypertrophy, " 
or  thickening  of  the  wall  with  diminution  in  the  size  of  the  cavity, 
is  a  fictitious  condition,  created  no  doubt  by  arrest  of  the  heart's 
action  during  systole  or  by  postmortem  ventricular  contraction. 


Normal 


Fig.  164. — Comparative  sizes  of  the  ventricles  in  a  normal  and  a  hypertrophied 
heart  (Philadelphia  General  Hospital). 

The  weight,  size,  and  shape  of  a  hypertrophied  heart  deviate 
from  the  normal  according  to  the  degree  and  site  of  the  enlargement. 
In  examples  of  moderate  hypertrophy  the  normal  average  weight  is 
commonly  doubled,  and  in  extreme  instances  is  exceeded  four-  or  five- 
fold, as  in  the  enormous  " ox-heart"  hypertrophy,  or  cor  boi'inum 
(Fig.  164).  Corresponding  increase  in  the  thickness  of  the  cardiac 
walls  develops,  even  in  eccentric  hypertrophies,  despite  the  apparent 
parietal  thinning  referable  to  the  coexisting  dilatation.  The  papillary 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM 


409 


muscles  and  the  muscular  columns  within  the  ventricles  are  thick- 
ened and  diminished  in  resiliency.  When  there  is  predominant  hy- 
pertrophy of  the  left  ventricle,  the  heart  becomes  elongated  and  the 
apex  unduly  blunt  and  displaced  downward  and  to  the  left;  when 
the  right  ventricle  is  enlarged,  the  contour  of  the  heart  becomes 
more  spherical  than  normal,  the  breadth  being  conspicuously 
increased  and  the  lengthening  less  apparent;  hypertrophy  of  both 
ventricles  causes  commensurate  elongation  of  the  organ,  with  unnat- 
ural flatness,  breadth,  and  bluntness  of  the  apex;  and  in  hypertrophy 
of  the  entire  heart  both  the  length  and  the  breadth  are  exaggerated, 


Fig.  164(1. — Radiograph  of  cardiac  hypertrophy  and  dilatation.     (Plate  by  Dr.  W.  F. 

Manges.) 

generally  with  approximate  preservation  of  the  normal  contour. 
Pure  hypertrophy  deepens  the  color  and  increases  the  consistence 
and  resistance  of  the  cardiac  muscle,  but  when  fibrous  and  fatty 
changes  coexist,  as  is  usually  the  case,  the  deep-red  color  of  the 
hypertrophy  becomes  correspondingly  paler,  and  the  muscle  under- 
goes more  or  less  fibrous  induration  and  fatty  softening.  The  his- 
tologic  changes  in  hypertrophy  consist  of  an  increase  in  the  size  of 


410  PHYSICAL   DIAGNOSIS 

the  individual  muscle-fibers,  and,  in  all  probability,  of  an  increase  in 
their  number. 

Left-sided  and  ventricular  hypertrophies  are  more  common  than 
right  sided  and  auricular,  the  four  chambers  of  the  heart  being 
affected  in  the  following  order  of  frequency:  left  ventricle,  right 
ventricle,  right  auricle,  and  left  auricle.  The  causes  of  cardiac 
hypertrophy  consist  of  arteriosclerosis,  valvular  and  parietal  affec- 
tions of  the  heart,  and  persistent  cardiac  overaction  due  to  various 
irritating  influences. 

General  hypertrophy  occurs  in  advanced  age  as  the  result  of  the 
increased  peripheral  resistance  incident  to  senile  arteriocapillary 
changes;  it  frequently  attends  myocardial  fibrosis  and  adherent 
pericardium,  which  mechanically  hamper  the  heart's  movements; 
and  it  develops  in  conditions  provocative  of  excessive  cardiac  fre- 
quency and  force — i.  e.,  the  tachycardia  and  palpitation  excited  by 
hyperthyroidism  ("kropfherz"),  by  the  neurosis  termed  paroxysmal 
tachycardia,  and  by  nicotin,  caffein,  and  sexual  excesses.  Alcohol 
is  an  active  cause  of  cardiac  hype'rtrophy,  since  it  not  only  stimulates 
the  cardiac  action  and  induces  arteriosclerosis,  but  also,  in  the  case 
of  those  who  consume  large  quantities  of  malt  liquors,  adds  to  the 
heart's  nutrition  and  increases  its  work  by  producing  hydremic 
plethora.  Prolonged  physical  exertion  eventually  leads  to  general 
hypertrophy,  but  especially  to  enlargement  of  the  left  ventricle. 
Primary  congenital  cardiac  hypertrophy  is,  according  to  Virchow,  in 
reality  a  diffuse  myomatous  neoplasia. 

Left  ventricular  hypertrophy  accompanies  aortic  stenosis,  aortic 
regurgitation,  and  mitral  regurgitation,  for  in  the  first  lesion  the 
ventricle  labors  hard  to  empty  its  contents,  and  in  the  other  two  it 
must  propel  an  excessive  volume  of  blood.  Stenosis  of  the  aorta 
and,  less  commonly,  aortic  aneurism,  when  they  impede  the  main 
arterial  current,  are  factors  of  left  ventricular  hypertrophy.  Arte- 
rial hypertension  in  combination  with  mitral  stenosis  produces  an 
extreme  grade  of  left  ventricular  hypertrophy,  even  greater  than 
that  ordinarily  met  with  in  arterial  sclerosis  plus  aortic  lesions  or 
chronic  nephritis  (Thomas  Lewis).  In  states  of  arterial  hyper- 
tension and  general  arterial  sclerosis  the  left  ventricle  hypertrophies 
to  overcome  increased  peripheral  resistance. 

Right  ventricular  hypertrophy  is  usually  traceable  to  obstruction  of 
the  pulmonary  circulation  resulting  either  from  mitral  defects  or 
from  pulmonary  cirrhosis,  emphysema,  or  widespread  pleural  adhe- 
sions; less  commonly,  obstruction  of  the  pulmonary  orifice  is  the 
cause  of  the  enlargement. 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  411 

Auricular  hypertrophy  is  invariably  attended  by  dilatation;  if  left- 
sided,  hypertrophy  of  the  auricle  means  mitral  disease,  especially 
stenosis ;  while  hypertrophy  of  the  right  auricle  is  generally  due  to 
intrapulmonary  hypertension  and  its  consequences,  or,  exceptionally, 
to  organic  tricuspid  lesions. 

Physical  Signs. — Left  Ventricular  Hypertrophy. — On  inspection 
the  precordia  may  appear  more  prominent  than  normal  if  the  subject 
be  a  child  (Fig.  40,  p.  89),  and  the  apex-beat,  which  is  violent  and 
unnaturally  extensive,  is  visibly  displaced  toward  the  left  and  down- 
ward. The  precordial  impulse  is  tumultuous,  the  arteries  throb 
excessively,  and  in  the  extreme  case  the  patient's  body  jogs  rhythm- 
ically with  every  beat  of  the  heart.  Palpation  demonstrates  the 
powerful  action  of  the  enlarged  heart,  whose  impact  is  appreciated 
as  a  deliberate,  heaving  thrust  which  counteracts  the  pressure  of  the 
examiner's  palm  and  distinctly  lifts  it  with  systole.  The  pulse 
indicates  high  arterial  tension,  and  is  full,  regular,  well  sustained, 
and  of  normal  or  somewhat  diminished  rate.  Percussion  reveals 
extension  of  the  cardiac  area,  vertically  upward,  horizontally  outward, 
and  obliquely  downward,  the  upper  limit  sometimes  reaching  to  the 
second  interspace,  the  left  border  extending  well  beyond  the  left 
midclavicular  line,  and  the  lower  margin  being  at  the  level  of  the 
sixth  or  seventh  interspace.  Auscultation  elicits  a  loud  and  prolonged 
mitral  first  sound  at  the  apex,  the  tone  in  this  situation  being  dis- 
tinguished by  the  dull  booming  quality  of  its  dominant  muscular 
component.  The  aortic  second  sound  is  greatly  accentuated,  being 
loud  and  clear  and  ringing.  In  the  event  of  unequal  intraventricular 
tension  (and  this  is  common),  the  second  sound  is  reduplicated,  and 
in  some  instances  there  is  also  doubling  of  the  first  sound.  In  pure 
hypertrophy,  to  which  the  foregoing  signs  apply,  murmurs  are  not 
audible. 

Right  Ventricular  Hypertrophy. — Inspection  discovers  systolic 
pulsation  in  the  epigastrium,  at  the  left  sternal  border  between  the 
fifth  and  seventh  costal  cartilages,  and  sometimes  at  the  right  sternal 
border  between  the  third  and  fifth  cartilages.  In  extreme  hypertrophy 
the  lower  sternal  region  and  the  apex  of  the  epigastrium  appear 
abnormally  prominent.  The  apex-beat  is  diffuse,  and  displaced 
horizontally  toward  the  left,  with  little  or  no  depression.  Palpation 
of  the  epigastrium  commonly  detects  a  heaving  impulse  just  below 
the  subcostal  angle,  most  extraordinarily  vigorous  thrusts  of  the 
ventricle  being  here  perceptible  in  the  emaciated  subject.  The 
transmitted  cardiac  impulse  occasionally  palpable  over  the  liver 
must  be  distinguished  from  true  hepatic  venous  pulsation  (q.  v.). 


412  PHYSICAL    DIAGNOSIS 

The  arterial  pulse,  aside  from  its  somewhat  diminished  volume, 
presents  no  noticeable  deviation  from  normal.  On  percussion  the 
precordial  limits  are  found  to  be  expanded  chiefly  in  a  horizontal 
direction  beyond  the  right  sternal  border,  dulling  the  normal  pul- 
monary resonance  of  the  cardiohepatic  angle  and  extending  i  inch 
(2.5  cm.)  or  so  to  the  right  of  this  landmark.  Auscultation  at  the 
tricuspid  area  shows  an  intense,  prolonged  first  sound,  and  at  the 
pulmonic  area  a  sharp,  intense,  sometimes  reduplicated  second 
sound.  Murmurs  do  not  arise,  of  course,  so  long  as  the  valvular 
mechanism  of  the  right  ventricle  remains  unimpaired. 

Auricular  Hypertrophy. — This  is  invariably  attended  by  dilatation 
of  these  chambers,  and  is  recognized  chiefly,  if  not  entirely,  by  the 
discovery  of  some  lesion  of  the  auriculoventricular  orifices  capable 
of  provoking  undue  intra-auricular  pressure.  Left  auricular  enlarge- 
ment cannot  be  diagnosed  by  objective  symptoms,  but  the  demon- 
stration of  mitral  disease  (especially  stenosis)  is  presumptive  evidence 
in  its  favor.  The  left  auricle,  in  exceptional  instances,  undergoes 
sufficient  hypertrophy  to  damp  the  pulmonary  vibrations,  and 
therefore  to  impair  percussion  resonance  at  the  left  of  the  cardiac 
base,  but  it  cannot  possibly  impinge  upon  the  anterior  chest-wall 
to  produce  visible  or  palpable  pulsations  thereupon,  as  is  sometimes 
carelessly  taught.  (Cf.  Mitral  Stenosis,  p.  443.)  Right  auricular 
enlargement  is  easier  to  distinguish,  since  well-marked  examples  are 
accompanied  by  presystolic  pulsation  near  the  sternal  ends  of  the 
third  and  fourth  right  interspaces,  by  encroachment  of  cardiac 
dulness  upon  this  territory,  and  by  a  forcible  jugular  pulse.  The 
character  of  this  venous  pulsation  is  accurately  fixed  by  the  sphygmo- 
gram,  which  indicates  an  exaggerated  wave  of  either  auricular  or  of 
ventricular  origin,  as  the  case  may  be.  (See  Figs.  132  and  133.)  The 
ability  to  auscultate  the  presystolic  tone  of  a  contracting  hyper- 
trophied  auricle,  right  or  left,  is  a  gift  possessed  by  few  clinicians. 
Enlargement  of  the  right  ventricle  and  the  signs  of  tricuspid  leakage 
or  obstruction,  particularly  the  former,  complete  the  clinical  picture 
sketched  by  the  signs  just  noted. 

Diagnosis. — Pure  cardiac  hypertrophy  is  betrayed  by  a  most 
distinctive  group  of  signs:  a  full,  regular,  high-tension  pulse,  a 
deliberate  heaving  precordial  impulse,  displacement  of  the  apex-beat, 
extension  of  the  cardiac  area,  and  a  prolonged,  muscular  mitral  or 
tricuspid  first  sound  with  ringing  accentuation  of  the  aortic  or 
pulmonic  second  sound.  The  chamber  or  chambers  chiefly  affected 
by  the  myocardial  overgrowth  can  be  identified  by  reviewing  more 
in  detail  the  objective  symptoms  above  enumerated.  This  can  be 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  413 

done  more  accurately  by  ordinary  physical  examination  than  by 
the  electrocardiograph,  which  gives  questionable  tracings  in  many 
instances.  It  is,  however,  the  rule  to  find  in  left  ventricular  hy- 
pertrophy inversion  of  the  R- wave  in  leads  II  and  III,  and  in 
right  ventricular  hypertrophy  either  a  normal  or  an  inverted 
R-\vave  in  lead  I  and  an  enlarged  R-vfave  in  leads  II  and  III. 

Simple  cardiac  overaction  may  counterfeit  hypertrophy,  in  so 
far  as  it  gives  rise  to  a  bounding  pulse,  strong  pulsation  of  the  pre- 
cordia  and  epigastrium,  and  intense  heart  sounds.  Here,  however, 
the  similarity  ends,  since  an  excited  heart  does  not  alter  the  position 
of  the  apex-beat  nor  enlarge  the  cardiac  area,  and,  furthermore,  as 
soon  as  the  heart  quiets  down  the  confusing  signs  disappear.  Bathy- 
cardia,  or  an  unnaturally  low  position  of  the  heart,  may  be  the 
cause  of  perceptible  epigastric  pulsation  of  excessive  force. 

The  question  of  hypertrophy  versus  cardiac  displacement  must  be 
settled,  when  the  apex  beats  away  from  its  natural  situation,  but 
if  mere  dislocation  exists,  the  cardiac  area,  despite  its  abnormal 
situation,  remains  of  normal  size  and  shape.  In  dealing  with  a  car- 
diac displacement,  moreover,  it  is  usually  possible  to  discover  the 
lesion  that  has  either  pushed  or  dragged  the  organ  from  its  accustomed 
position.  (See  p.  318.) 

Pulmonary  cirrhosis,  whereby  the  anterior  margins  of  the  lungs 
may  be  retracted  so  as  to  expose  the  parietal  surface  of  the  heart, 
is  sometimes  attended  by  vigorous  precordial  pulsation,  by  increase 
in  the  area  of  cardiac  flatness,  and  by  exaggeration  of  the  cardiac 
sounds.  In  favor  of  this  condition,  rather  than  of  true  hypertrophy, 
are  the  absence  of  a  typical  booming  first  sound  and  of  a  ringing 
second  sound,  the  failure  to  detect  tumultuous  action  of  the  arteries, 
the  inability  to  discover  a  satisfactory  factor  of  hypertrophy,  and 
the  presence  of  definite  pulmonary  signs.  If  displaced,  the  heart 
tends  to  ride  upward  and  toward  the  left,  as  the  result  of  traction 
from  these  directions.  In  this  connection  it  is  well  to  recall  the  fact 
that  cirrhosis  of  the  lungs  in  time  induces  right  ventricular  hyper- 
trophy and,  ultimately,  distention  of  this  chamber.  In  the  presence 
of  extensive  pulmonary  emphysema  it  is  sometimes  impossible  to 
elicit  the  physical  signs  of  an  enlarged  heart,  owing  to  the  mass  of 
dilated  vesicular  tissue  which  separates  the  heart  from  the  chest-wall. 
Apparent  enlargement  of  tlte  heart,  due  to  extension  of  its  surface 
limits,  may  depend  upon  paracardial  lesions,  such  as  consolidation 
of  the  anterior  pulmonary  borders,  circumscribed  pleural  effusion, 
mediastinal  tumor,  and  aneurism  of  the  aortic  arch,  though  under 
such  circumstances  careful  analysis  of  the  subject's  history  and 


414  PHYSICAL   DIAGNOSIS 

physical  signs  suffices  for  an  accurate  differentiation.  The  same 
is  true  of  certain  thoracic  deformities  that  may  cause  undue  promi- 
nence of  the  precordial  region. 

The  discrimination  between  pericardial  effusion  and  a  heart  enlarged 
by  dilated  hypertrophy  has  been  discussed  under  the  former  affection. 
(See  p.  401.) 

CARDIAC  DILATATION 

Clinical  Pathology. — Dilatation  of  the  heart,  or  an  abnormal 
enlargement  of  one  or  more  of  its  chambers,  is  due  to  stretching  of 
its  wall  under  the  stress  of  overwork  in  excess  of  the  organ's  nutrition 
and  muscular  power.  Intracardiac  hypertension  and  diminished 
parietal  resistance,  singly  or  combined,  are  the  essential  factors 
which  force  the  cardiac  muscle  to  give  way  in  this  manner,  either 
suddenly  in  consequence  of  an  acute  strain,  or  gradually  after  a 
prolonged  period  of  overwork.  In  the  great  majority  of  instances 
the  resistance  of  the  myocardium  is  weakened  by  structural  changes 
such  as  parenchymatous  degeneration  and  interstitial  fibrosis,  but 
in  others  simple  exhaustion  of  the  cardiac  muscle  appears  to  be  the 
sole  predisposing  cause  of  the  dilatation. 

Dilatation  may  exist  alone  or  in  combination  with  hypertrophy, 
and,  like  the  latter,  may  be  either  a  general  or  a  partial  change. 
Dilatation  with  thinning  consists  of  an  enlargement  of  the  chamber 
with  thinning  of  its  wall,  generally  of  acute  development,  and  pri- 
marily excited  by  a  sudden  rise  of  pressure  within  the  heart. 
Thus,  acute  distention,  particularly  of  the  right  heart,  some- 
times results  from  the  sudden  increase  of  blood-pressure  incident 
to  inordinate  muscular  strain;  the  myocardium  may  suddenly  yield 
and  the  corresponding  chamber  dilate  under  the  intracardiac  hyper- 
tension and  overdistention  due  to  traumatic  valvular  insufficiency; 
and  acute  dilatation  may  occur  whenever  the  resistance  of  the 
myocardium  is  lessened  by  nutritive  defects,  and  by  the  action  of 
bacterial  toxins. 

Dilatation  with  hypertrophy  denotes  enlargement  of  the  chamber 
with  increase  in  the  cardiac  musculature,  the  wall  being  either  of 
normal  or  of  increased  thickness.  This  type  of  dilatation,  save  when 
a  degenerated  hypertrophied  heart  suddenly  gives  way  under  acute 
strain,  is  essentially  a  chronic  condition,  and  intimately  associated 
with  hypertrophy,  of  which  it  usually  represents  the  secondary  phase. 
Pure  hypertrophy  of  the  heart  has  certain  limitations,  fixed  by  nutri- 
tion, beyond  which  the  overgrowth  must  cease  and  undergo  retro- 
grade changes,  for  want  of  adequate  blood-supply  through  the 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  415 

coronary  arteries,  either  because  these  vessels  are  atheromatous  or 
because  of  the  rapid  and  disproportionate  increase  in  the  volume 
of  the  cardiac  muscle.  When  this  limit  is  reached,  the  cardiac 
wall  yields  to  increased  pressure  from  within,  so  that  to  the  primary 
hypertrophy  dilatation  is  now  added.  When  finally  dilatation  can 
go  no  further,  for  to  this  change  also  there  must  be  a  limit,  the  chamber 
surrounded  by  the  weakened  muscle  fails  to  empty  itself  with  systole, 
is  in  consequence  still  more  distended  by  residual  blood,  and  becomes 
the  starting-point  of  a  stasis  affecting  that  part  of  the  circulatory 
system  behind  the  dilated  chamber.  This  means  failure  of  compensa- 
tion, the  immediate  effects  of  which  are  relative  mitral  leakage,  left 
auricular  dilatation,  and  engorgement  of  the  lungs  when  the  left 
ventricle  fails,  and  tricuspid  insufficiency,  sooner  or  later  followed 
by  right  auricular  dilatation  and  general  venous  stasis,  when  the 
right  ventricle  yields.  These  accidents  and  the  consequences 
thereto  are  considered  in  connection  with  lesions  of  the  cardiac 
valves.  (See  p.  427.)  In  favorable  cases  primary  dilatation 
of  a  cardiac  chamber  is  followed  by  hypertrophy  of  its  wall,  in 
order  thus  to  compensate  for  the  impairment  of  cardiac  strength, 
the  duration,  extent,  and  efficiency  of  this  increased  muscular 
power  depending  upon  the  circumstances  prevailing  in  the  individual 
instance.  So  long  as  the  hypertrophy  predominates  sufficiently 
to  ensure  complete  systolic  discharge  of  the  ventricular  contents, 
stasis  is  warded  off  and  the  circulation  does  not  suffer,  but  so  soon  as 
myocardial  degeneration  and  intracardiac  hypertension,  one  or  both, 
become  the  prevailing  change,  secondary  dilatation,  leading  to 
permanent  circulatory  embarrassment,  inevitably  supervenes. 

Physical  Signs. — Left  Ventricular  Dilatation. — Inspection  shows 
enfeeblement  of  the  apex-beat,  which  is  displaced  downward  and  to 
the  left  of  iJS  normal  site.  The  impulse  is  either  diffuse,  forceless, 
and  undulatory,  or,  in  advanced  dilatation,  quite  imperceptible  to 
the  eye.  On  palpation  the  apical  impulse,  if  at  all  palpable,  can 
be  but  vaguely  felt  as  a  somewhat  abrupt  tapping  or  slapping  beat, 
utterly  unsustained  and  lacking  in  strength.  It  is  a  common  experi- 
ence to  encounter  a  visible  apex-beat  which  cannot  be  palpated. 
The  pulse  is  rapid,  arhythmic,  and  of  diminished  volume  and  tension, 
the  individual  waves  being  diminutive  and  easily  extinguished  by 
moderate  pressure  on  the  vessel  (Fig.  165).  Percussion  defines  an 
enlarged  cardiac  outline  whose  upper,  lateral,  and  lower  limits 
virtually  correspond  to  those  of  left  ventricular  hypertrophy  (q.  v.). 
On  auscultation  the  heart  sounds  are  found  to  be  feeble,  impure, 
arhythmic,  and  perhaps  modified  by  coexistent  murmurs.  The 


41 6  PHYSICAL   DIAGNOSIS 

first  sound  at  the  apex  is  short,  sharp,  and  high  pitched,  having  lost 
most  of  its  muscular  tone,  and  acquired  a  valvular  quality  like  that 
of  the  second  sound.  In  the  event  of  serious  ventricular  failure 
these  two  sounds,  so  accoustically  alike,  may  be  approximated  by 
an  abbreviated  diastolic  period,  so  as  to  reproduce  the  fetal  cardiac 
rhythm-  termed  embryocardia,  while  in  some  instances  the  irregularity 
conforms  to  the  triple  beat  of  gallop  rhythm.  (See  pp.  362  and  371.) 
The  tricuspid  first  sound  shows  no  noteworthy  deviation  from 
normal.  At  the  base  of  the  heart  the  aortic  second  sound  is  weakened 
commensurately  with  the  gravity  of  the  left  ventricular  enfeeblement, 
while  the  pulmonic  second  sound,  so  long  as  the  right  ventricle  is 
unimpaired,  is  relatively  accentuated.  Endocardial  murmurs, 
when  present,  generally  indicate  relative  mitral  leakage,  though 


Fig.  165. — Synchronous  sphygmographic  tracings  of  the  carotid  artery  and  the  apex- 
beat  in  a  case  of  cardiac  dilatation.   (Tracing  by  Dr.  G.  Bachmann.) 

preexisting  valvular  disease  should  always  be  credited  as  a  possible 
factor  of  the  bruits. 

Right  Ventricular  Dilatation. — On  inspection  and  palpation  one 
may  note  suppression  of  the  normal  apex-beat  and  undulatory 
pulsation  corresponding  to  the  parietal  impact  of  the  enlarged 
flaccid  ventricle:  below  and  on  either  side  of  the  ensiform;  outside 
the  right  sternal  border  between  the  fourth  and  seventh  costal  car- 
tilages; and  close  to  the  left  sternal  margin  between  the  second  and 
fifth  cartilages  (Fig.  125,  p.  321).  The  arterial  pulse  is  affected  by 
attendant  conditions  more  than  by  the  ventricular  dilatation,  being 
usually  of  increased  frequency,  small  volume,  disturbed  rhythm, 
and  low  tension;  the  venous  pulse,  in  the  face  of  free  tricuspid  leakage, 
produces  a  sphygmogram  having  a  high,  blunt  z/-wave  of  the  systolic 
or  ventricular  type.  (See  Fig.  133,  p.  349.)  Percussion  defines  the 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  417 

right  border  of  the  heart  well  beyond  the  right  sternal  edge,  with 
moderate  horizontal  extension  of  the  cardiac  area  toward  the  left 
midclavicular  line.  On  auscultation  a  more  or  less  faint,  abbreviated, 
sharply  valvular  tricuspid  first  sound  is  audible,  and  at  the  base  the 
pulmonic  second  sound  is  enfeebled  and  obscure.  The  systolic 
bruit  of  relative  tricuspid  incompetence,  with  its  striking  attendant 
phenomena  of  venous  stasis,  is  not  unlikely  to  be  a  dominant  physical 
sign,  confirmative  of  the  foregoing  findings. 

Auricular  Dilatation. — The  physical  signs  of  this  condition  have 
been  referred  to  on  page  412,  under  its  attendant  change,  auricular 
hypertrophy.  In  this  connection  it  may  be  added  that  in  the  study 
of  auricular  enlargements  the  venous  pulse  tracing  is  most  helpful 
in  determining  to  what  extent  and  in  what  manner  the  integrity  and 
power  of  these  cardiac  chambers  have  become  affected. 

Diagnosis. — The  diagnosis  of  cardiac  dilatation  rests  upon  the 
following  distinctive  signs:  a  feeble,  wavy  precordial  impulse,  an 
ill-defined,  displaced  apex-beat,  a  small,  rapid,  irregular  arterial 
pulse,  enlargement  of  the  cardiac  outline,  and  a  weak  though  sharp 
first  sound  with  an  enfeebled  second  sound.  The  other  evidence, 
relating  to  failing  compensation  and  to  back  pressure  and  its  conse- 
quences, is  detailed  in  connection  with  valvular  defects  (see  p.  432), 
and  therefore  need  not  be  reconsidered  here. 

Dilatation  and  hypertrophy,  save  for  the  enlargement  of  the  cardiac 
area  common  to  both,  are  attended  by  diametrically  opposed  physical 
signs,  as  enumerated  at  length  above.  In  attempting  to  judge  which 
process  predominates  in  an  example  of  combined  hypertrophy  and 
dilatation,  one  should  be  guided  mainly  by  a  minute  analysis  of  the 
cardiac  sounds,  by  the  presence  or  absence  of  relative  regurgitant 
murmurs,  by  the  condition  of  the  arterial  and  venous  pulses,  and  by 
a  study  stasis  of  phenomena.  Pericardial  effusion  has  been  contrasted 
with  dilatation  of  the  heart  on  page  401. 

MYOCARDITIS     (Carditis;    Granular    Myocardial    Degeneration;   Myo- 

cardial    Fibrosis;    Myocardial    Abscess) 

Clinical  Pathology. — Acute  Myocarditis. — Under  acute  diffuse 
inflammations  of  the  myocardium  it  is  convenient  to  include  in  one 
group  certain  degenerative  processes  primarily  affecting  the  muscular 
fibers,  and  in  another  group  acute  inflammations  of  the  interstitial 
tissue,  the  former  being  designated  as  parenchymatous,  and  the 
latter  as  interstitial,  myocarditis. 

Acute  parenchymatous  myocarditis  is  to  every  intent  and  purpose 
identical  with  the  condition  known  as  "cloudy  swelling"  or  "granular 
27 


41 8  PHYSICAL   DIAGNOSIS 

degeneration"  of  the  heart,  in  which  the  muscular  fibers  become 
swollen,  lose  their  striation,  and  are  loaded  with  albuminoid  granula- 
tions, the  heart  muscle  in  consequence  acquiring  a  dull  gray  appear- 
ance and  an  abnormally  soft  and  edematous  consistence.  A  slight 
degree  of  interstitial  inflammation  usually  attends  this  predominant 
parenchymatous  change,  which,  if  unchecked,  inevitably  leads  to  fatty 
degeneration.  Parenchymatous  inflammation  of  the  myocardium, 
toxic  in  origin,  is  a  familiar  cardiac  complication  in  many  active 
febrile  and  infectious  states — i.  e.,  septicemia,  enteric  fever,  pneu- 
monia, rheumatic  fever,  scarlatina,  gonorrhea,  influenza,  and  insola- 
tion; it  arises  in  connection  with  exhausting  cachexias;  and  it  is 
sometimes  consequent  to  endo-  and  pericarditis. 

Acute  interstitial  myocarditis,  also  referable  to  acute  infections  and 
to  inflammations  of  the  endo-  and  pericardium,  consists  of  an  infil- 
tration of  the  interstitial  tissue  with  small  round  cells  and  leukocytes, 
together  with  vascular  dilatation,  and  a  variable  degree  of  degenera- 
tion of  the  muscular  fibers.  This  produces  unnatural  softening  and 
grayish  discoloration  of  the  heart,  either  uniformly  or  locally,  depend- 
ing upon  whether  the  inflammation  is  diffuse  or  circumscribed.  A 
mild  interstitial  myocarditis  may  undergo  perfect  resolution,  leaving 
the  cardiac  muscle  undamaged,  but  severe  cases  probably  terminate 
in  unalterable  fibroid  myocarditis. 

Acute  suppurative  myocarditis  is  generally  due  to  the  lodgment  of 
infected  thrombi  in  the  branches  of  the  coronary  artery,  less  commonly 
to  the  direct  extension  of  a  pyogenic  lesion  of  the  endocardium  or 
the  pericardium.  Various  septic  processes,  such  as  malignant  endo- 
carditis, osteomyelitis,  septic  phlebitis,  and  puerperal  fever,  are  the 
primary  factors  of  this  grave  condition.  The  suppurative  foci  range 
in  size  from  minute  miliary  points  to  abscesses  as  large  as  a  centimeter 
or  more  in  diameter,  and  may  be  either  widely  disseminated  through 
the  entire  myocardium  or  restricted  and  circumscribed,  notably  to 
the  anterior  wall  of  the  left  ventricle.  If  small  and  few,  the  pus  foci 
may  become  inspissated,  absorbed,  and  cicatrized  or  calcified,  but 
if  there  be  extensive  suppuration,  and  the  subject  survives,  aneurism 
of  the  cardiac  wall  is  a  possible  sequel.  Or  the  pus  may  penetrate  the 
pericardial  sac  or  ulcerate  into  one  of  the  cavities  of  the  heart,  exciting 
in  the  former  instance  fatal  purulent  pericarditis,  and  in  the  latter, 
metastatic  abscesses  of  remote  organs  contaminated  by  septic  emboli 
carried  by  the  ventricular  blood  streams.  An  interseptal  abscess 
may,  by  erosion,  establish  a  communication  between  the  ventricles 
or  the  auricles. 

Chronic  Myocarditis. — This  type  of  heart  disease,  most  common 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  419 

in  men  of  middle  or  advanced  age,  consists  of  a  chronic  interstitial 
inflammation  of  the  myocardium  terminating  in  fibroid  induration. 
Usually  the  process  is  chronic  from  its  inception,  but  sometimes 
it  is  the  sequel  of  an  acute  myocardial  inflammation  or  degeneration. 
Disease  of  the  coronary  arteries  is  undoubtedly  the  leading  factor  of 
chronic  myocarditis,  which  ordinarily  is  the  result  of  the  nutritive 
defects  consequent  to  obliterative  endarteritis,  although  occasionally 
an  area  of  anemic  necrosis,  referable  to  arterial  thrombosis,  is  the 
starting-point  of  the  lesion.  In  other  cases  the  myocardial  changes 
are  due  to  the  direct  extension  of  chronic  endocarditis  or  pericarditis, 
with  predominant  implication  of  the  papillary  muscles  in  the  former 
event  and  of  the  outer  surface  of  the  myocardium  in  the  latter. 
Fibrosis  of  the  heart  muscle  is  part  and  parcel  of  the  retrograde 
changes  incident  to  advanced  age;  it  is  excited  by  the  irritant  action 
of  circulating  toxic  substances,  as  in  rheumatic  fever,  malarial  fever, 
syphilis,  and  as  in  alcoholism,  nicotin-poisoning,  plumbism,  gout, 
diabetes,  and  nephritis;  it  develops  after  various  acute  infectious 
diseases,  doubtless  as  a  sequel  of  a  primary  interstitial  myocarditis 
of  intense  grade;  and,  most  exceptionally,  it  arises  traumatically, 
as  from  an  injury  to  the  precordia. 

The  fibrosis  may  be  so  extensively  distributed  as  to  merit  the  term 
diffuse,  or,  as  is  more  frequently  the  case,  it  may  be  more  or  less 
restricted,  especially  to  the  apical  portion  of  the  left  ventricular  wall, 
to  the  interventricular  septum,  and  to  the  papillary  muscles;  in 
congenital  cardiofibrosis,  however,  the  apex  of  the  right  ventricle  is 
the  favorite  site  of  the  lesion.  The  affected  areas  are  recognized 
as  linear  stripes  and  rounded  patches  of  grayish-white  induration, 
composed  of  connective-tissue  bands  paralleling  the  muscle-fibers, 
which  eventually  atrophy,  undergo  granular  and  fatty  degeneration, 
and  perhaps  become  wholly  obliterated,  in  consequence  of  com- 
pression by  the  overgrowth.  In  rheumatic  myocarditis  the  myo- 
cardial nodules  of  Aschoff  are  commonly  found,  existing  as  discrete 
microscopic  areas  of  leukocytes  and  embryonal  tissue,  tending 
ultimately  to  form  scars,  and  situated  usually  in  the  subendocardial 
parts  of  the  septum  in  the  left  ventricular  wall. 

Associated  changes  of  myocardial  fibrosis  include  pressure  stenoses 
of  the  aortic  and  pulmonary  orifices  produced  by  cicatricial  contrac- 
tions; mitral  and  tricuspid  leakages  due  to  fibroid  shortening  of  the 
papillary  muscles;  chronic  valvulitis  and  pericarditis;  and  obliter- 
ative endarteritis  of  the  coronary  vessels.  Hypertrophy  and  dila- 
tation are  common  sequels,  but  of  these  changes  the  attendant 
arteriosclerosis,  valvular  defects,  and  pericarditis  are  also  im- 


420  PHYSICAL   DIAGNOSIS 

portant  factors;  or  hypertrophy  may  occur  merely  as  a  com- 
pensatory overgrowth  of  the  non-fibrous  parts  of  the  muscle. 
In  cases  of  advanced  myocardial  disease  there  is  a  tendency  toward 
thrombosis  within  the  chambers  of  the  heart,  particularly  in  the 
auricular  appendages  and  in  the  ventricles  near  the  apex.  Aneurism 
of  the  heart  may  arise,  if  a  circumscribed  patch  of  fibrosis  becomes 
so  weakened  by  degenerative  changes  that  finally  it  yields  and 
bulges  under  the  incessant  strain  of  intracardiac  pressure. 

Physical  Signs. — Inspection. — In  acute  forms  of  the  disease  the 
patient's  pallor,  apathy,  and  breathlessness  constitute  a  most  sug- 
gestive trio  of  objective  signs,  or  there  may  be  a  cyanotic  counte- 
nance which  betrays  a  lagging  circulation.  Subjects  of  myocardial 
fibrosis  are  notably  affected  by  shortness  of  breath  and  distressing 
palpitation  upon  slight  exertion.  In  suppurative  myocarditis  one 
should  look  for  profound  depression,  collapse,  symptoms  of  sepsis, 
and  evidences  of  septic  infarcts;  and  precordial  pain  is  not  un- 
usual in  this  type  of  myocardial  inflammation. 

Palpation. — Enfeeblement  of  the  cardiac  impulse  and  a  forceless, 
empty,  and  often  arhythmic  pulse-beat  are  discovered  by  precordial 
and  radial  palpation,  and,  if  there  be  considerable  venous  stasis, 
the  liver  and  the  spleen  become  palpably  enlarged.  In  chronic  cases 
a  slow  pulse  is  the  rule,  except  in  the  event  of  advanced  fatty  changes 
or  dilatation,  which  provoke  undue  rapidity  and  weakness  of  the  beats. 

Percussion. — Unnatural  extension  of  the  cardiac  area,  particularly 
in  a  horizontal  direction,  is  found  in  cases  associated  with  decided 
dilatation  of  the  heart,  but,  naturally,  this  helpful  clue  to  the  recogni- 
tion of  the  myocardial  damage  is  forthcoming  only  in  advanced 
cases. 

Auscultation. — The  tones  of  the  heart  are  enfeebled,  muffled,  and 
impure  in  accordance  with  the  gravity  of  the  existing  cardiac  asthenia. 
Ordinarily  the  muscular  sound  is  indistinct  or  even  inaudible,  so  that 
the  valvular  quality  of  the  heart's  sounds  predominates;  or,  as 
sometimes  happens,  the  valvular  tone,  too,  is  suppressed,  in  which 
event  it  is  difficult  to  auscultate  any  distinct  cardiac  sounds  whatever. 
The  systolic  murmur  of  a  relative  mitral  leakage,  from  stretching 
of  the  valve  ring,  is  not  uncommonly  audible  at  the  apex,  and,  should 
endocarditis  or  pericarditis  coexist,  the  adventitious  sounds  of  these 
complications  are  also  appreciable. 

Diagnosis. — Acute  myocardial  degeneration  is  the  natural  inference 
when,  during  the  course  of  an  acute  infectious  process,  dyspnea, 
pallor,  vomiting,  and  precordial  oppression  and  distress  supervene, 
along  with  a  rapid  pulse  of  low  tension  and  a  muffled  impurity  of 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  421 

the  cardiac  sounds.  The  discovery  of  a  systolic  (relative)  murmur 
at  the  apex,  of  the  percussion  findings  of  ventricular  dilatation,  and 
of  evidences  of  venous  stasis  change  such  an  inference  to  a  reasonable 
certainty.  Suppurative  myocarditis,  though  rarely  diagnosed  cor- 
rectly during  life,  is  suggested  by  extreme  severity  of  the  constitutional 
symptoms,  by  the  existence  of  a  septic  etiologic  factor,  and  by  the 
occurrence  of  embolic  processes. 

Chronic  interstitial  myocarditis  is  prone  to  affect  middle-aged  men 
whose  arteries  have  become  sclerotic  from  the  immoderate  use  of 
alcohol  or  from  the  effect  of  syphilis,  gout,  or  similar  poisons  to  the 
cardiovascular  system.  Or  it  may  attack  the  clean-lived  man  of 
affairs  long  subject  to  the  stress  of  a  strenuous  business  or  pro- 
fessionaL  routine.  In  such  subjects  the  important  diagnostic 
details  consist  of  hardening  of  the  palpable  arteries;  a  persistently 
high-tension  pulse  commonly  deviating  from  the  normal  rate  and 
rhythm;  a  comparatively  feeble  first  apical  sound  of  valvular  quality 
and  perhaps  masked  by  a  systolic  murmur  of  mitral  leakage;  ringing 
accentuation  of  the  aortic  second  sound,  not  infrequently  attended 
by  a  systolic  murmur  of  aortic  atheroma  and  dilatation;  and  extension 
of  precordial  flatness  indicative  of  enlargement  of  the  left  ventricle 
and  of  the  ascending  part  of  the  aorta.  In  advanced  cases  the 
supervention  of  dilatation  may  transform  the  foregoing  picture  into 
one  of  cardiac  breakdown.  Other  evidences,  of  arteriosclerotic 
character,  that  may  be  associated  with  the  cardiac  signs  comprise 
interstitial  nephritis,  glycosufia,  anginal  paroxysms,  intermittent 
lameness,  and  certain  cerebral  symptoms,  such  as  vertigo,  recurrent 
attacks  of  transient  aphasia,  palsy,  and,  exceptionally,  of  the  Stokes- 
Adams  syndrome — bradycardia,  syncope,  and  convulsions. 

ACUTE   ENDOCARDITIS  (Valvulitis;  Acute  Mural  Endocarditis) 

Clinical  Pathology. — Acute  inflammation  of  the  endocardium, 
implicating  chiefly  the  valves  but  to  a  less  extent  the  mural  serosa, 
may  occur  clinically  as  a  simple  benign  type  or  as  a  malignant  process. 
In  this  connection,  however,  one  should  recall  Osier's  assertion,  that 
"so-called  benign  endocarditis  kills  in  the  long  run  a  very  much 
larger  number  of  persons  than  the  malignant  form, "  for  endocarditis, 
if  it  be  not  immediately  perilous,  tends  to  become  so  ultimately,  in 
consequence  of  the  sclerotic  changes  thereby  provoked.  Further- 
more, there  is  no  clear-cut  pathologic  demarcation  between  the  two 
forms  of  inflammation,  since  they  represent  but  different  grades  of 
intensity  of  the  same  infectious  process. 


422  PHYSICAL   DIAGNOSIS 

Rheumatic  infection  is  par  excellence  the  factor  of  acute  endocarditis, 
and  the  vast  majority  of  instances  are  traceable  to  this  poison,  either 
in  its  frank  arthritic  form  or  in  some  one  of  its  guises — tonsillar, 
choreic,  or  cutaneous.  Conservatively,  it  is  safe  to  believe  that  in 
adults  articular  rheumatism  inflames  the  endocardium  in  from 
25  to  35  per  cent,  of  all  cases,  and  that  in  children  this  incidence  is 
doubled.  Other  causes  that  may  light  up  an  endocarditis  include 
certain  septic  and  pyemic  processes:  erysipelas,  gonorrhea,  osteomye- 
litis, puerperal  fevers,  infected  wounds,  abscess;  and  many  of  the 
specific  fevers,  such  as  pneumonia,  diphtheria,  scarlatina,  influenza, 
tuberculosis,  and,  less  commonly,  other  infectious  and  eruptive 
diseases.  As  a  terminal  infection  there  is  no  doubt  that  a  mild  grade 
of  endocardial  inflammation  commonly  develops,  nor  is  there  any 
doubt  that  traumatism,  unless  attended  by  bacterial  invasion,  never 


Fig.  1650. — Electrocardiogram  of  a  case  of  acute  endocarditis,  showing  deep  Q- 
depression,  large  .R-wave,  inverted  T-wave.  and  irregular  prolongation  of  T,  R  interval. 
(Tracing  by.  Dr.  T.  A.  Cope.) 

excites  a  vegetative  endocarditis.  Valve  leaflets  habitually  exposed 
to  the  irritant  effect  of  arterial  hypertension  are  particularly  prone 
to  become  inflamed  and  vegetative.  The  streptococcus,  staphylococ- 
cus,  pneumococcus,  and  gonococcus  are  the  germs  that  have  an 
especially  close  causal  relation  to  endocarditis,  while  less  commonly 
the  lesion  is  excited  by  such  bacteria  as  the  bacillus  of  tuberculosis, 
influenza,  or  enteric  fever,  or  by  some  other  specific  microorganism. 
Simple  acute  endocarditis,  as  a  rule,  attacks  the  valves  of  the  left 
side  of  the  heart,  the  mitral,  aortic,  tricuspid,  and  pulmonic  structures 
being  affected  in  the  order  of  frequency  named.  Lesions  of  the  right 
side  of  the  heart  are  generally  of  intrauterine  origin,  but  it  is  proba- 
ble that  right-sided  endocarditis  during  postuterine  life  is  not  such  a 
rarity  as  was  once  supposed,  though  signs  of  such  a  condition  are  not 
frequently  found,  owing  to  the  relatively  greater  tendency  of  reso- 
lution to  occur  in  lesions  of  the  tricuspid  and  pulmonic  valves  (v.  i.). 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM  423 

Simple  acute  endocarditis  has  a  special  predilection  for  the  lines 
of  valve  contact  a  short  distance  (about  yV  inch  or  2  mm.)  from 
the  free  margins,  the  auricular  surface  of  the  mitral  leaflets  and 
the  ventricular  aspect  of  the  aortic  cusps  usually  showing  the 
earliest  and  most  advanced  alterations,  which  are  primarily  those 
of  endothelial  degeneration  and  are  structurally  of  thrombotic  char- 
acter. The  affected  valves  are  the  seat  of  local  endothelial  necroses, 
the  swollen,  abraded,  and  roughened  surfaces  becoming  covered 
with  a  deposit  of  granular  or  fibrillar  fibrin  permeated  by  proliferating 
connective  tissue  and  by  infiltrated  leukocytes.  The  vegetations 
developed  in  this  manner  appear  as  delicate  or  as  coarse  excrescences 
attached  to  the  valves,  and,  if  recent,  of  pinkish  color  and  friable 
texture,  or,  if  old,  pale  and  of  hard,  warty  consistence.  Such  vegeta- 
tions, if  small,  soft,  and  delicately  globular,  merit  the  term  beaded 
excrescences;  those  of  greater  size,  denser  character,  and  cauliflower- 
like  or  warty  in  form  are  well  described  as  verrucose  excrescences; 
and  those  of  inordinate  size  and  polypoid  contour  are  referred  to  as 
villous  or  polypous  lesions.  The  tissues  of  the  affected  valves  show 
more  or  less  inflammatory  damage,  leading  to  a  corresponding 
degree  of  thickening,  contraction,  and  puckering  of  the  leaflets, 
whereby  orificial  stenosis  and  incompetence  arise.  Rarely,  a  simple 
acute  endocarditis  of  the  benign  type  undergoes  resolution  and  leaves 
the  valve  functionally  perfect;  or  it  may  undergo  extensive  necrotic 
and  ulcerative  changes;  but  ordinarily  it  results  in  the  unalterable 
structural  deformities  distinctive  of  chronic  valvular  disease.  The 
detachment  of  a  valve  thrombus  or  of  a  bit  of  necrotic  tissue  is  a 
cause  of  embolism.  Apart  from  the  local  lesion,  acute  endocarditis 
sets  up  a  variable  grade  of  myocardial  inflammation  and  degenera- 
tion, which,  indeed,  may  do  more  harm  than  the  valvular  defects. 
Pericarditis  is  also  a  familiar  associated  lesion — Sturges  found  it  in 
94  per  cent,  of  cases  in  children,  and  in  view  of  the  frequency  with 
which  endo-myo-pericarditis  coexists  he  purposes  to  apply  the 
term  carditis  to  the  majority  of  acute  endocardi tides;  or  the  term 
pancarditis,  suggested  by  Jiirgensen,  seems  even  more  appropriate. 
Laceration  of  a  valve,  rupture  of  a  tendinous  cord,  aortitis,  pleuritis, 
and  pneumonitis  are  other  possible  complications,  the  first  three 
being  most  exceptional. 

Ulcerative  or  malignant  endocarditis  is  generally  due  to  strepto- 
coccal,  staphylococcal,  pneumococcal,  or  gonococcal  infection,  and, 
though  commonly  left  sided,  implicates  the  right  heart  more  fre- 
quently than  does  simple  benign  endocarditis.  The  process  is  one 
of  predominant  necrosis  and  of  subordinate  repair,  leading  to  exten- 


424 


PHYSICAL   DIAGNOSIS 


sive  and  irreparable  structural  damage.    This  may  take  the  form  of 
ulcerative  erosion  resulting  in  more  or  less  complete  destruction  of 


Fig.  1 66. — Malignant  endocarditis,  with  extensive  implication  of  aortic  valves  (Phila- 
delphia General  Hospital). 

one  or  more  valve  cusps,  in  valve  fenestration  and  aneurism,  and 
in  rupture  of  chordae  tendineae;  or  ulcers  may  perforate  a  valve 
ring,  produce  septal  perforation,  and,  penetrating  the  mural  endo- 
cardium, set  up  a  suppurative  myopericarditis,  perhaps  terminating 
in  cardiac  aneurism  or  in  rupture  of  the  heart.  Septic  embolism 
is  a  grave  danger  associated  with  a  mycotic  process  of  this  sort.  In 
other  cases  the  ulcerative  changes  are  overshadowed  by  the  formation 
of  luxuriant  vegetations  springing  from  the  valve  mechanism  and 
from  the  mural  endocardium,  the  vegetative  outgrowths  commonly 
being  attended  by  deep  necrosis.  If  not  leading  to  an  immediately 
fatal  outcome,  the  excrescences  sometimes  proliferate  to  a  most 
extraordinary  extent  and  ultimately  may  become  coated  with  an 
unyielding,  rigid  deposit  of  lime  salts. 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  425 

Physical  Signs. — Inspection. — In  the  average  case  of  simple 
endocarditis  there  are  no  visible  evidences  of  the  lesion,  unless,  as 
exceptionally  happens,  the  myocardial  damage  is  grave  enough  to 
displace  the  apex-beat  and  to  alter  its  force.  It  is  in  malignant  cases 
particularly  that  signs  of  cardiac  dilatation  are  likely  to  be  observed, 
and  in  these  instances  the  subject  may  show  the  inroads  of  profound 
septic  poisoning. 

Palpation. — Suggestive,  but  by  no  means  characteristic,  informa- 
tion is  occasionally  afforded  by  palpation.  So  long  as  myocardial 
integrity  is  unimpaired  palpation,  of  course,  shows  nothing,  but  in 
the  case  of  an  acute  valvulitis  grafted  upon  an  old  valvular  lesion 
abnormal  variations  in  the  force,  extent,  and  site  of  the  apex-beat, 
sometimes  a  thrill,  and  perhaps  hepatic  enlargement  are  to  be  looked 
for.  The  pulse  is  commonly  increased  in  frequency,  especially  in 
febrile  subjects,  and  may  be  altered  in  volume,  in  tension,  and  in 
rhythm. 

Percussion. — Routine  percussion  of  the  cardiac  areas,  particularly 
those  overlying  the  ventricles,  is  indicated  in  every  suspected  case  of 
endocardial  inflammation,  irrespective  of  its  benignancy  or  malig- 
nancy, in  order  thus  to  be  able  to  detect  the  first  indications  of 
ventricular  dilatation.  In  the  absence  of  this  change  the  percussion 
findings  indicate  no  alteration  in  the  extent  of  the  normal  cardiac 
outline. 

Auscultation. — The  earliest  definite  physical  sign  of  simple  acute 
endocarditis,  in  the  great  majority  of  instances,  consists  of  an  impurity 
of  the  first  cardiac-sound  at  the  apex,  followed  by  a  muffled  prolonga- 
tion of  the  tone,  and  finally  succeeded  by  the  development  of  a 
distinct,  though  usually  soft  and  blowing,  systolic  murmur  which  is 
clearly  conducted  as  far  as  the  patient's  axilla,  and  in  time  is  attended 
by  accentuation  of  the  pulmonic  second  sound.  This  transition  from 
a  murmurish  tone  to  an  actual  bruit  having  a  well-defined  area  of 
propagation  points  to  mitral  regurgitation,  the  most  common  con- 
sequence of  this  type  of  endocardial  disease.  Less  commonly,  a 
muffled  aortic  second  sound  similarly  is  converted  into  a  diastolic 
murmur,  or  the  rough  bruit  of  mitral  stenosis  may  appear.  The 
mere  presence  of  a  murmur,  especially  if  it  be  basal,  does  not  mean 
endocarditis,  for  such  a  sound  is  quite  as  likely  to  be  anemic  or 
relative  as  it  is  to  be  endocarditic.  The  criterion,  then,  is  not  the 
murmur,  so  much  as  the  sequence  of  tonal  changes  attending  its 
development.  Furthermore,  the  inability  to  hear  a  murmur  does 
not  exclude  valvulitis,  which,  if  it  does  not  fulfil  certain  physical 
conditions,  creates  no  vibrations  of  the  blood  column. 


426  PHYSICAL   DIAGNOSIS 

Malignant  endocarditis  may  afford  auscultatory  signs  identical 
with  those  of  the  benign  form,  or  there  may  be  none  at  all.  In  certain 
cases,  however,  characterized  by  extensive  and  highly  virulent  endo- 
cardial  damage,  there  are  single  or  multiple  murmurs  peculiar  in 
their  tendency  to  change  in  puncta  maxima,  and  in  rhythm,  intensity, 
and  quality,  affecting,  as  they  do  so,  the  character  of  the  other  cardiac 
sounds.  To  a  single  mitral  murmur,  for  example,  may  suddenly 
be  added  an  aortic  bruit,  as  the  mycotic  process  bridges  the  short 
endocardial  path  separating  the  two  orifices.  Myocardial  impair- 
ment of  the  cardiac  tones,  the  dry  rub  of  pericardial  inflammation, 
and  the  friction-sound  of  pleurisy  are  important  consecutive  findings 
in  malignant  infection  of  the  endocardium. 

Diagnosis. — In  acute  simple  endocarditis  the  gradual  supervention 
of  a  murmur  attended  by  undue  intensity  of  the  pulmonic  second 
sound  and  by  signs  of  myocardial  weakness  is  the  chief  diagnostic 
clue,  which,  unfortunately,  is  not  available  in  every  case.  Due 
attention  must  also  be  paid  to  other  suggestive  clinical  findings,  such 
as  moderate  fever,  rapidity  of  the  pulse,  precordial  uneasiness 
(rarely,  actual  pain),  and  more  or  less  respiratory  oppression;  while 
the  patient's  history,  present  and  previous,  is  to  be  interrogated 
with  a  view  to  finding  some  factor  of  endocardial  inflammation — 
rheumatism,  tonsillitis,  pneumonia,  or  similar  infectious  process. 
The  distinction  between  true  endocarditic  murmurs  and  the  adven- 
titious sounds  due  to  anemia,  to  relative  incompetence,  and  to  plastic 
pericarditis  is  considered  at  sufficient  length  in  connection  with  these 
conditions.  (See  pp.  379  and  391.) 

In  certain  cases  of  malignant  endocarditis  the  development  of 
erratic,  changeable  murmurs  and  of  cardiac  dilatation  in  an  unmis- 
takably septic  subject  provides  satisfactory  evidence  of  an  endo- 
cardial ulceration.  But  in  cases  that  do  not  conform  to  this  cardiac 
type  the  local  signs  may  be  most  equivocal,  so  that  one  must  turn 
elsewhere  for  definite  data,  which  in  general  refer  to  a  condition  of 
septic  poisoning  and  in  particular  to  pyemia,  to  the  typhoid  state, 
and  to  meningeal  inflammation,  according  to  the  existing  individual 
peculiarities.  In  studying  such  a  varied  symptomatology  it  is 
important  first  to  discover  the  presence  of  some  septic  factor,  either 
local  or  general,  and  to  identify,  by  blood-culturing,  the  infective 
agent,  after  which  investigation  of  the  systemic  damage  wrought 
thereby  is  in  order.  This  inquiry  should  be  directed  toward  the 
presence  or  absence  of  chills,  remittent  pyrexia,  progressive  anemia, 
rapid  wasting,  extreme  exhaustion,  splenic  enlargement,  leukocyto- 
sis,  iodophilia,  and  evidences  of  septic  embolism.  There  is  also  a 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  427 

puzzling  group  of  cases  that  shows  little  else  than  moderate,  often 
recurrent,  fever  and  splenic  enlargement,  together  with  clear  signs  of 
chronic  valvular  disease.  These  cases,  which  may  be  acute,  chronic, 
or  relapsing  in  type,  are  especially  liable  to  embolic  accidents,  and 
probably  represent  an  active  necrotic  process  implanted  upon  a 
preexisting  valvular  sclerosis. 

Enteric  fever  may  closely  resemble  malignant  endocarditis,  in 
general  symtomatology  and  in  the  existence  of  an  endocardial 
(relative)  murmur.  Apart  from  the  patient's  previous  history,  these 
data  bespeak  typhoid:  prodromal  indisposition,  gradual  onset 
without  a  true  rigor,  relatively  late  prostration,  specific  findings 
from  blood-cultures  and  from  the  serum  test,  and  the  orderly  appear- 
ance of  the  distinctive  symptom-complex  of  enteric  fever  by  the  end 
of  the  first  week. 

M alarid  fever,  although  it  may  superficially  ape  malignant  endo- 
carditis, can  scarcely  prove  a  source  of  serious  confusion,  in  the  face 
of  its  distinctive  hematologic  picture — leukopenic  mononucleosis,  free 
pigment,  and  the  malarial  hemameba. 

CHRONIC    ENDOCARDITIS     (Chronic     Valvular     Disease?    Chronic 
Interstitial   Endocarditis) 

Clinical  Pathology. — Chronic  inflammation  of  the  valvular  and 
mural  endocardium  occurs  both  as  a  sequel  of  acute  endocarditis 
and  as  a  primary  chronic  sclerosis,  in  either  event  leading  to  de- 
formities of  the  valves  and  orifices  whereby  regurgitant  and  stenotic 
lesions  arise,  and  also  to  permanent  alterations  in  the  structure  and 
functional  efficiency  of  the  cardiac  muscle.  More  than  one-half 
of  all  chronic  valvular  defects  are  traceable  to  rheumatic  poison, 
and  especially  in  childhood  and  in  young  adult  life  is  this  irritant 
the  cause  of  the  original  endocardial  inflammation.  Langmead 
found  signs  of  endocarditis  in  87  per  cent,  of  133  rheumatic  school 
children,  and  in  approximately  3  per  cent,  of  2556  children  ex- 
amined, regardless  of  their  past  medical  history. 

Less  commonly  the  permanent  lesions  are  due  to  an  acute 
endocarditis  excited  by  some  one  of  the  numerous  other  factors 
referred  to  above.  In  the  type  of  chronic  valvular  disease  arising 
as  a  slow  fibrosis  the  damage  generally  can  be  laid  at  the  door  of 
alcohol,  syphilis,  and  muscular  strain,  which,  singly  or  in  combina- 
tion, subject  the  valve  mechanism  to  irritation  by  circulating  toxins 
and  by  excessive  arterial  tension.  Arteriosclerosis,  nephritis,  gout, 
malaria,  diabetes,  and  plumbism  act  similarly. 

The  special  manner  in  which  the  different  valves  are  affected  by 
chronic  endocarditis  and  the  important  secondary  cardiac  changes 


428  PHYSICAL   DIAGNOSIS 

thereby  set  up  are,  for  convenience  sake,  considered  in  connection 
with  the  several  types  of  individual  valvular  lesions.  (See  p.  434 
el  seq.)  It  is  sufficient  here  to  summarize  the  pathologic  findings 
of  chronic  valvular  disease  as  follows:  (a)  Fibrosis,  induration,  and 
thickening  of  the  valves  and  of  their  musculotendinous  attachments; 
(6)  contraction  of  the  hyperplasia,  resulting  in  curling  and  puckering 
of  the  valve  edges,  shortening  and  thickening  of  the  chordae  tendineae 
and  papillary  muscles,  and  orificial  deformity,  whereby  faulty 
approximation  of  the  cusps  arises;  (c)  adhesion  of  the  valve  edges, 
restricting  their  movements  and  causing  obstruction  and  leakage  at 
the  orifices  they  guard;  (d)  impregnation  of  the  sclerotic  structures 
with  lime-salts,  still  further  adding  to  their  rigidity  and  mechanically 
interfering  with  their  normal  movement;  (e)  sclerotic  thickening 
and  calcification  of  the  mural  endocardium.  The  valves  thus 
damaged  are  sometimes  found  to  be  beaded  with  simple  inflammatory 
excrescences,  and  are  prone,  in  the  event  of  bacterial  invasion,  to 


Aortic 

III.  Regurgitation 
IV.  Stenosis 


Mitral 

I.  Regurgitation 

II.  Stenosis 


Fig.  167. — Relative  incidence  of  regurgitant  and  stenotic  lesions  of  the  mitral  and 

aortic  valves. 


become  attacked  by  a  malignantly  necrotic  process,  or,  if  exposed  to 
sudden  violent  strain,  may  rupture.  Myocardial  degeneration  and 
inflammation  are  practically  constant  associated  lesions  which,  as 
intimated  before,  give  more  concern  to  the  clinician  than  do  the 
underlying  valvular  defects. 

Types  and  Relative  Incidence  of  Valvular  Lesions. — A  valvular 


DISEASES   OF    THE   CARDIOVASCULAR   SYSTEM  429 

defect  acting  as  a  barrier  to  the  onward  flow  of  blood  is  known  as 
a  stenosis,  or  an  obstruction,  and  a  deformity  preventing  the  tight 
closure  of  a  valve,  and  thus  permitting  backward  leakage  through 
the  orifice  into  the  chamber  immediately  behind,  is  designated  as  a 
lesion  of  regurgitation,  incompetence,  or  insufficiency.  Valvular 
lesions  may  be  single,  but  more  commonly  they  are  either  double  or 
combined,  a  single  lesion  being  either  stenosis  or  regurgitation  of  one 
orifice,  a  double  lesion  meaning  both  stenosis  and  regurgitation  at 
one  orifice,  and  a  combined  lesion  consisting  of  two  or  more  defects 
at  different  orifices. 

The  valves  of  the  left  side  of  the  heart  are  much  more  frequently 
implicated  than  those  of  the  right  side,  defects  of  the  tricuspid  and 
pulmonic  leaflets  usually  arising  as  sequels  of  left-sided  disease,  and 
but  exceptionally  representing  acquired  primary  processes.  Con- 
genital valvular  disease  is  right  sided  in  the  vast  majority  of  instances. 
Mitral  regurgitation  is  by  all  odds  the  most  common  single  valvular 
defect,  after  which  follow,  in  this  order  of  frequency,  mitral  stenosis, 
aortic  regurgitation,1  and  aortic  stenosis  (Fig.  167).  The  relative 
incidence  of  organic  right-sided  defects  reads:  tricuspid  regurgi- 
tation, tricuspid  stenosis,  pulmonary  stenosis,  and  pulmonary  regurgi- 
tation. Of  combined  lesions,  F.  J.  Smith  has  worked  out  this  order 
of  frequency:  double  aortic  and  mitral  regurgitation;  aortic  and 
mitral  stenosis;  aortic  and  mitral  regurgitation;  double  aortic  and 
double  mitral. 

The  comparative  frequency  of  valvular  defects  at  the  four  different 
cardiac  orifices  is  illustrated  by  the  following  table,  based  upon  the 
analysis  of  nearly  4000  collected  cases: 

, , .     ,                  .                     Mitral  and  Pulmonic 

Lockhart  Gillespie.                                                              Aortic.  Tricuspid. 

(1914  cases.)  58.5  per  cent.  21.4  per  cent.  19.2  per  cent.  0.8  per  cent. 
T.  G.  Ashton. 

(1024  cases.)  60.6        "          21.5         "          17.0        "  i.o        " 
Parrot. 

(1058  cases.)  58.6        "          35.9        "          0.5 

From  other  data  given  by  these  and  other  authors,  notably  F.  J. 
Smith  and  Middleton,  too  elaborate  for  quotation  here,  these  general 
facts  relating  to  chronic  valvular  disease  may  be  deduced: 

i.  Including  both  sexes,  mitral  disease  constitutes  more  than 
one-half  of  all  cases;  in  men  less  than  one-half,  and  in  women  more 
than  three-fourths  of  valvular  lesions  are  mitral. 

1  It  is,  perhaps,  questionable  which  of  these  two  defects  is  the  more  common, 
for  their  incidence  is  practically  about  the  same.  Most  statistics,  however, 
show  that  mitral  stenosis  is  a  shade  the  more  frequent. 


43° 


PHYSICAL   DIAGNOSIS 


2.  Including  both  sexes,  aortic  disease  constitutes  about  one-fifth 
of  all  cases;  it  is  three  times  as  common  in  men  as  it  is  in  women. 

3.  Double  or  combined  lesions  are   found  in  about  one-fifth  of 
all  cases;  they  are  almost  twice  as  common  in  men  as  in  women. 

4.  Right-sided  lesions  constitute  less  than  one  one-hundredth  of 
the  total  cases  of  valvular  disease. 

Primary  Effects  of  Valvular  Lesions. — In  health  the  blood  flows 
unimpeded  through  the  chambers  of  the  heart  into  the  arterial, 
capillary,  and  venous  channels,  and  thence  back  into  the  heart. 
Not  only  does  the  stream  always  flow  in  the  same  direction,  but  with 
each  systole  exactly  the  right  volume  of  blood  is  emptied  into  the 
arterial  system  by  the  contracting  ventricles,  to  maintain  perfect 
circulatory  equilibrium.  This  is  ensured  so  long  as  the  valves 
open  and  close  properly  and  the  size  of  the  orifices  remains  normal, 
but  the  balance  is  immediately  disturbed  when  valvular  defects 
develop,  which  either  obstruct  the  onward  flow  of  the  blood-stream 
or  permit  its  reflux. 

Valvular  defects,  whether  they  obstruct  the  blood-stream  or  allow 
it  to  regurgitate,  primarily  cause  accumulation  and  stasis  of  blood 
in  the  chamber  of  the  heart  immediately  back  of  the  crippled  valve, 
with  the  result  that  this  chamber  becomes  habitually  overdistended 
and  dilated.  The  muscular  walls  then  hypertrophy,  in  consequence 
of  the  increased  work  demanded  of  them,  but  ultimately  they  again 
tend  to  dilate,  as  they  sooner  or  later  weaken  under  the  continued 
strain.  The  chamber  primarily  affected  then  gives  out  completely, 
and  the  back  pressure  extends  to  the  other  parts  of  the  cardiovascular 
system,  step  by  step.  The  predominance  of  one  or  the  other  of  these 
structural  changes  in  the  cardiac  muscle  depends  upon  the  peculiar- 
ities of  the  determining  lesion  and  upon  the  extent  and  character  of 
the  retrograde  changes  in  the  myocardium.  These  influences  will 
be  discussed  presently,  in  connection  with  the  individual  valvular 
lesions. 

A  condition  of  compensation  is  said  to  exist  so  long  as  the  heart 
adequately  responds  to  the  demands  made  upon  it  to  overcome,  by 
increased  work,  the  stress  imposed  by  valvular  defects.  Thus,  by 
virtue  of  its  reserve  force,  the  heart  enlarges  so  as  to  equalize  the 
circulatory  disturbance  by  overcoming  the  stasis,  and  the  conservative 
change,  compensatory  hypertrophy,  supervenes  (Fig.  168,  //).  Perfect 
compensation  continues  so  long  as  the  nutrition  of  the  myocardium 
is  sufficient  to  allow  the  development  of  hypertrophy  adequate  to 
maintain  a  normal  cardiovascular  equilibrium,  and  at  this  stage  of 
a  valvular  disease  the  cardiac  physical  signs  are  the  sole  evidences  of 
the  lesion  to  be  detected.  It  is  important  to  bear  in  mind  the  fact 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM 


431 


that  during  this  period  of  perfect  compensation  drugs  are  not  only 
not  indicated,  but  their  use  may  be  distinctly  injurious,  no  matter 
what  be  the  character  of  the  cardiac  defect.  Ruptured  or  broken  com- 
pensation supervenes  when  the  nutrition  and  reserve  force  of  the 
heart  fail  to  keep  pace  with  the  strain  imposed  by  the  valvular  lesion, 
so  that  the  circulatory  balance  becomes  disturbed  and  the  stasis 
aggravated.  It  is  a  change  referable  to  myocardial  enfeeblement 
and  ultimate  dilatation  of  the  heart  which  develops,  either  gradually 
or  abruptly,  when  the  nutrition  of  the  heart  becomes  so  impaired 
that  this  muscle  relaxes  under  the  stress  which  hitherto  it  has 
been  able  to  bear,  and  hence  the  total  available  cardiac  force  is 


force  reyiund^_ 
to  preserve 
Compensation. 


r/y/Jtrtrofiluf 
fteseroe  force. 


Reserve  TZree. 


Ordinary 
force. 


jr. 

Fig.  1 68. — The  effects  of  adequate  and  of  ruptured  compensation  upon  the  force 
of  the  heart:  7,  Normal  cardiac  force;  //,  excess  of  cardiac  force  attending  stage  of 
adequate  compensation;  ///,  deficiency  of  cardiac  force  incident  to  stage  of  ruptured 
compensation. 

inadequate  for  the  maintainance  of  the  normal  circulatory  balance 
(Fig.  168,  III). 

Ruptured  compensation  is  betrayed  not  so  much  by  distinctive 
cardiac  physical  signs  as  by  groups  of  symptoms,  more  or  less  urgent, 
indicating  circulatory  derangements  in  different  organs.  For 
example,  in  left-sided  valvular  disease  the  brunt  of  the  strain  is  felt 
by  the  lungs  which  become  engorged  as  soon  as  the  stasis  and  high 
tension  extend  backward  from  the  left  auricle  and  reach  the 
pulmonary  circulation.  Later  the  congestion,  via  the  pulmonary 
circuit,  affects  the  right  side  of  the  heart,  and  ultimately  extends  even 
beyond  its  confines  into  the  venae  cavae,  causing  general  venous 
engorgement. 


432 


PHYSICAL    DIAGNOSIS 


Secondary  Effects  of  Valvular  Lesions. — The  secondary  effects  of 
valvular  disease  develop  in  consequence  of  the  back  pressure  of  blood, 


Subclavian  vein 


Pulmonary  artery 


Venae  cavae 


Renal  veins  —  "v 


Hepatic  veins 
Portal  vein    — 


Subclavian  artery 


—    Aorta 

Pulmonary  veins 


—  Renal  artery 

—  Gastric  arteries 


-  —  Splenic  artery 


,  _  Superior  mesenteric 
artery 


.       Inferior  mesenteric 
artery 


Iliac  veins 


Hiac  arteries 


Fig.  169. — Mechanism    of    the   stasis   phenomena   secondary  to  chronic  valvular 

disease. 


which  in  course  of  time  causes  venous  congestion  of  different  organs 
and  parts  of  the  body  remote  from  the  crippled  heart.  These  signs 
of  stasis  are  referred  to  the  respiratory  system,  the  gastro-intestinal 


DISEASES  OF  THE   CARDIOVASCULAR   SYSTEM 


433 


tract,  the  kidneys,  the  brain,  and  the  great  venous  trunks.    The 
mechanism  by  which  these  changes  arise  is  illustrated  in  the  accom- 


Fig.  170. — Appearance  of  a  subject  of  chronic  valvular  disease  during  the  stage  of 
failing  compensation  (Jefferson  Hospital). 

panying  diagram  (Fig.  169),  and  their  recognition  may  be  facilitated 
by  referring  to  the  following  symptom-groups: 


Bronchopulmonary: 


Castro-intestinal: 


Renal: 
Cerebral: 


Venous: 


28 


Cough;  dyspnea;  orthopnea;  hemoptysis;  bronchitis; 
edema  of  lungs;  passive  congestion  of  lungs;  hydro- 
thorax. 

Chronic  gastric  and  intestinal  catarrh;  hematemesis; 
melena;  hemorrhoids. 

Enlarged,  tender,  and  pulsating  liver;  icterus.  Enlarged 
and  tender  spleen. 

Urine  scanty,  high  specific  gravity,  high  color,  and  con- 
taining albumin,  urates  in  excess,  and  tube  casts. 

Headache;  vertigo;  faintness;  syncope;  phosphenes; 
insomnia;  unpleasant  dreams;  drowsiness;  delirium. 

Embolism;  thrombosis;  cerebral  hemorrhage. 

Cyanosis  of  face  and  extremities;  clubbed  fingers.  Sys- 
tolic jugular  pulsation.  Edema  of  extremities;  ascites; 
anasarca. 


434 


PHYSICAL   DIAGNOSIS 


The  special  pathology,  physical  signs,  and  diagnosis  of  the  several 
varieties  of  chronic  valvular  disease  will  now  be  considered  with 
relation  to  the  individual  lesions. 

MITRAL   REGURGITATION 

Clinical  Pathology. — This,  the  most  common  of  all  organic 
valvular  lesions,  is  usually  acquired  during  childhood,  doubtless 
because  at  this  period  of  life  factors  of  endocarditis,  such  as  rheuma- 
tism, chorea,  tonsillitis,  the  exanthemata,  and  other  infections,  are 
prevalent.  Less  commonly  leakage  at  the  mitral  orifice  depends 
upon  arteriosclerotic  changes  supervening  in  later  life,  as  the  result 
of  nephritis,  gout,  syphilis,  or  the  habitual  use  of  alcohol.  Traumatic 


Cavity  of  left  auricle 
Fig.  171. — Mitral  regurgitation  (Jefferson  Hospital  Laboratories). 

injury  of  the  valve  is  a  potential  source  of  mitral  regurgitation,  and" 
congenital  defects,  in  the  exceptional  instance,  account  for  the 
incompetency. 

Interference  with  the  accurate  apposition  of  the  mitral  valve 
curtains  results  in  imperfect  closure  of  the  mitral  orifice,  and,  in 
consequence,  leakage  of  blood  from  the  ventricle  into  the  auricle 
takes  place  during  ventricular  systole.  This  condition  of  mitral 
regurgitation  is  due  fundamentally  either  to  organic  derangement  of 
the  valve  mechanism  or  to  muscular  changes  in  the  wall  of  the  left 
ventricle,  singly  or  combined.  In  the  organic  type  (Fig.  171} 


DISEASES    OF   THE   CARDIOVASCULAR    SYSTEM  435 

endocarditic  induration  and  contraction  of  the  mitral  leaflets,  with 
thickening,  eversion,  and  fusion  of  their  edges  and  perhaps  adhesion 
to  the  ventricular  wall,  are  ordinarily  responsible  for  the  faulty 
closure  of  the  mitral  orifice.  Or  the  latter  may  leak  because  the 
cusps  are  prevented  from  closing  tight  by  vegetations  upon  their 
surface,  by  the  projection  of  calcareous  plates  at  their  base,  or  by 
sclerosis  and  contraction  of  the  mitral  ring.  In  extreme  examples 
the  valvular  structures  at  the  mitral  orifice  are  virtually  converted 
into  a  dense  calcareous  mass,  and  in  this  event  there  is  obviously 
stenosis  as  well  as  regurgitation  at  the  auriculoventricular  opening. 
The  foregoing  changes  are  attended  by  more  or  less  shortening  and 
fibrocalcareous  degeneration  of  the  tendinous  cords  and  papillary 
muscles,  which  possibly  may  even  rupture.  Exceptionally  a  valve 
leaflet  is  the  seat  of  laceration,  fenestration,  or  so-called  aneurism. 
In  the  muscular  type  the  leakage  is  due  not  to  structural  damage  to  the 
valves  but  to  enlargement  of  the  auriculoventricular  orifice  and 
to  defective  muscular  action  incident  to  myocardial  enfeeblement  and 
dilatation  of  the  left  ventricle.  Febrile  conditions,  anemia,  and 
myocardial  inflammation  and  degeneration,  by  interfering  with 
cardiac  nutrition,  are  likely  to  cause  this  type  of  degeneration,  which 
also  may  arise  in  consequence  of  ventricular  enlargement  secondary  to 
habitual  arterial  hypertension  or  to  aortic  valvular  lesions.  Relative 
incompetence  develops  as  the  result  of  left  ventricular  dilatation,  the 
mitral  orifice  being  so  stretched  that  its  valve  curtains  fail  to  close 
tightly,  and  the  ventricular  walls  being  so  distended  as  to  drag  upon 
the  musculotendinous  attachments  of  the  valve  segments  and  hence 
to  prevent  their  perfect  approximation.  It  is  likely  that  the 
reflux  thus  permitted,  if  adequately  accommodated  by  the  pul- 
monary circulation,  relieves  the  stress  of  a  laboring  left  heart, 
by  a  mechanism  comparable  to  that  of  the  well-known  "safety- 
valve  action"  at  the  tricuspid  orifice  in  distention  of  the  right  ven- 
tricle. (See  p.  463.)  Muscular  incompetence  also  may  occur 
primarily  from  feeble  ventricular  systole,  a  defect  leading  to 
insufficient  constriction  of  the  mitral  orifice  and  to  deficient 
action  of  the  papillary  muscles,  by  fault  of  which  systolic  back- 
ward leakage  of  blood  is  permitted  through  the  inadequately 
guarded  mitral  orifice. 

As  the  result  of  mitral  insufficiency  both  a  normal  supply  of  blood 
from  the  pulmonary  veins  and  a  reflux  stream  from  the  ventricle 
pour  into  and  together  overdistend  the  left  auricle,  which  in  con- 
sequence dilates,  and,  since  expulsion  of  this  large  blood  mass  means 
additional  effort,  the  auricular  wall  also  undergoes  compensatory 


43 6  PHYSICAL   DIAGNOSIS 

hypertrophy.  The  left  ventricle  becomes  similarly  dilated  and 
hypertrophied,  for  of  necessity  it  must  receive  and  expel  an  abnor- 
mally great  volume  of  blood.  As  the  result  of  the  auricular  sur- 
charging there  are  stasis  and  hypertension  of  the  pulmonary  circu- 
lation attended  by  dilatation,  and,  even  by  atheroma  of  the  vessels, 
and  finally,  by  brown  induration  of  the  lungs.  By  fault  of  the  pul- 
monary engorgement  the  right  ventricle  is  so  strained  and  overworked 
that  it  dilates  and  hypertrophies,  and  when,  after  a  variable  period, 
the  limit  of  hypertrophy  is  reached  and  dilatation  predominates, 
the  tricuspid  valve  leaks,  permitting  systolic  regurgitation  into  the 
right  auricle,  which  in  turn  dilates  and  hypertrophies  in  an  endeavor 
to  compensate  the  venous  resistance.  Hand  in  hand  with  this 
embarrassment  of  the  right  heart,  systemic  venous  congestion  pro- 
gresses, sooner  or  later  to  set  up  chronic  catarrh  of  the  mucosal 
surfaces,  transudative  accumulations  in  the  serous  sacs  and  sub- 
cutaneous tissue,  and  visceral  engorgement  and  induration.  The 
cardiac  muscle,  meanwhile,  enfeebled  by  the  combined  effects  of 
undernutrition  and  overwork,  is  the  seat  of  fibrous  and  fatty  degen- 
eration. 

Physical  Signs. — Inspection. — So  long  as  the  cardiac  strength  is 
adequate  the  patient's  appearance  is  not  suggestive  of  any  valvular 
defect,  but  with  the  onset  of  venous  stasis  and  failing  compensation, 
dyspnea,  cyanosis,  especially  of  the  lips,  nose,  and  fingers,  cough, 
watery  or  blood-streaked  expectoration,  and  dropsy  form  a  familiar 
group  of  objective  symptoms.  In  cases  of  considerable  chronicity 
one  expects  also  to  find  more  or  less  dilatation  of  the  superficial  veins 
of  the  face  and  upper  chest,  clubbing  of  the  finger-tips,  emaciation, 
and  a  facies  picturing  anemic  pallor,  an  ashen-gray  hue,  or  an  icteroid 
staining. 

The  cardiac  impulse  is  unnaturally  extensive,  and  displaced 
downward  and  to  the  left  as  the  result  of  the  left  ventricular  enlarge- 
ment, while  if  the  right  ventricle  be  hypertrophied  there  is  visible 
epigastric  pulsation.  Exceptionally,  in  young  children  the  hyper- 
trophy is  sufficient  to  produce  outward  bulging  of  the  precordia,  but 
in  adults  no  such  deformity  occurs. 

Palpation. — The  impulse  over  the  enlarged  ventricles  is  either 
forcible  and  heaving  or  weak  and  undulatory,  according  to  whether 
hypertrophy  or  dilatation  predominates;  over  the  liver  there  may  be 
distinct  pulsation,  due  in  most  instances  to  the  violent  impact  of  the 
right  ventricle,  but  in  some  produced  by  the  transmission  of  a  systolic 
venous  pulse.  Palpation  over  or  just  above  the  cardiac  apex  some- 
times, but  by  no  means  constantly,  appreciates  a  delicate  systolic 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM  437 

thrill,  which  is  the  tactile  equivalent  of  the  murmur  heard  on  aus- 
cultation. In  examples  of  extreme  regurgitation  it  is  sometimes 
possible  to  detect,  by  palpation  of  the  chest-wall,  diffuse  pulsation 
of  the  lungs — the  so-called  "pulmonary  pulse." 

The  radial  pulse,  save  perhaps  for  slight  acceleration  and  hypo- 
tension, remains  practically  normal  until  the  left  ventricle  fails,  but 
when  this  happens  the  beats  become  notably  deficient  in  volume, 
inordinately  rapid,  and  irregular  in  rhythm  and  force.  Ineffectual 
systole,  or  an  occasional  ventricular  contraction  too  feeble  to  produce 
a  radial  impulse,  is  not  infrequently  detected  by  simultaneous  palpa- 
tion of  the  precordia  and  the  wrist.  The  sphygmogram  of  such  a 
pulse  well  illustrates  its  striking  irregularity  and  low  tension,  the 
incidence  of  the  curves  being  most  erratic  and  their  height  unequal, 
with  a  vertical  upstroke,  sharp  apex,  rapidly  falling  downstroke, 
and  low  dicrotic  wave.  (See  Fig.  130,  in  and  vii;  p.  340.) 

Percussion. — The  area  of  cardiac  dulness  is  increased  horizontally 
and  downward  toward  the  left,  owing  to  the  bilateral  ventricular 
enlargement,  and  occasionally  it  is  possible  to  map  out  an  upward 
extension  of  the  basic  outline  corresponding  to  the  situation  of  an 
enlarged  left  auricle.  The  size  of  the  hepatic  and  splenic  percussion 
areas  is  increased,  as  the  result  of  venous  obstruction. 

Auscultation. — Mitral  regurgitation  gives  rise  to  systolic  murmur 
at  or  near  the  apex,  whence  the  sound  is  transmitted  toward  the  left, 
usually  into  the  axilla  and  sometimes  as  far  backward  as  the  inferior 
angle  of  the  left  scapula  (Fig.  1 54) .  The  clear  propagation  of  the 
sound  toward  the  left  depends  upon  the  good  conducting  proper- 
ties of  the  chordae  tendineae,  the  papillary  muscles,  and  the  ven- 
tricular wall,  and  upon  the  efficiency  of  the  mural  vibratory  path 
formed  by  the  chest-wall. 

Typically,  the  punctum  maximum  of  this  murmur  is  at  the 
clinical  apex  of  the  heart,  from  which  point  the  sound  gradu- 
ally grows  fainter  as  the  stethoscope  is  moved  beyond  the  limits 
of  the  precordia,  but  exceptionally  the  murmur  is  so  loud  as  to  be 
audible  far  beyond  these  confines.  In  rare  instances  a  mitral  systolic 
murmur  is  heard  most  distinctly  along  the  left  sternal  border,  usually 
between  the  fourth  and  sixth  costal  cartilages,  but  occasionally  as 
high  as  the  second  interspace.  The  murmur  of  a  mitral  leakage  is 
more  likely  to  be  soft  and  blowing  than  harsh  or  rasping,  and  its 
distinctness  is  decidedly  affected  by  the  subject's  posture,  the  sound 
often  being  clearer  when  the  patient  is  recumbent.  The  duration  of 
the  murmur  is  variable:  it  may  absolutely  coincide  with  the  first 


438  PHYSICAL   DIAGNOSIS 

sound,  perhaps  through  only  the  first  part  of  this  period,  or  occur 
in  the  latter  portion  of  systole,  in  which  case  a  moderate  grade  of 
incompetence  is  suggested  (Sahli).  The  longer  the  bruit  the  more 
conspicuous  its  diminuendo  character,  and  the  shorter  the  sound 
the  more  pronounced  its  "whiffy"  quality. 

The  first  sound  at  the  apex  is  partly  or  wholly  replaced  by  the 
attendant  murmur,  and  within  certain  limits  it  is  true  that  the 
greater  the  degree  of  the  regurgitation  the  more  effectually  its  bruit 
masks  the  first  sound  of  the  heart,  which  may,  indeed,  be  quite 
inaudible.  Accentuation  of  the  pulmonic  second  sound,  due  to 
pulmonary  congestion,  is  a  valuable  corroborative  sign  of  mitral 
disease,  while  reduplication  of  the  second  sound  at  the  cardiac  base, 
from  unequal  tension  within  the  two  ventricles,  is  of  some  significance. 

Diagnosis. — A  systolic  apical  murmur  propagated  toward  the 
left  axilla,  accentuation  of  the  second  pulmonic  sound,  and  bilateral 
ventricular  enlargement  are  the  cardinal  signs  of  mitral  regurgitation. 
These  signs,  unmistakable  during  the  stage  of  compensation,  are 
more  or  less  obscured  later,  when  cyanosis,  dropsy,  erratic  action  of 
the  heart,  and  other  signals  of  cardiac  break-down  dominate  the 
clinical  picture. 

In  relative  mitral  leakage  versus  the  organic  type,  the  physical 
signs  are  often  an  uncertain  guide,  since  if  the  mitral  orifice  be  widely 
stretched  by  a  dilated  left  ventricle,  the  thrill,  murmur,  and  loud 
pulmonic  second  sound  of  an  endocarditic  reflux  will  be  faithfully 
reproduced.  Rosenbach's  statement,  that  a  late  systolic  murmur 
invariably  means  an  organic  structural  defect  of  the  left  auriculo- 
ventricular  opening,  is  helpful,  but  the  clinical  history,  the  question 
of  secondary  signs,  and  the  subsequent  behavior  of  the  essential 
cardiac  findings  must  largely  mold  the  final  decision.  Most  rela- 
tive mitral  murmurs,  however,  are  comparatively  quiet,  poorly 
conducted,  evanescent,  unattended  by  accentuation  of  the  pul- 
monic second  sound,  and  unaccompanied  by  congestion  of  the 
lungs  and  of  the  right  heart.  They  commonly  develop  in  debili- 
tated, anemic  subjects  during  the  course  of  some  acute  febrile  in- 
fection or  other  exhausting  disease  that  induces  myocardial  weak- 
ness, and  the  bruit  completely  vanishes  when  the  tone  of  the 
cardiac  muscle  is  restored.  In  a  type  of  cardiac  enfeeblement 
known  as  "Copenhagen  heart"  (Hielscher),  common  among  ha- 
bitual users  of  strong  snuff,  relative  mitral  insufficiency  is  readily 
provoked  by  exercise,  and  frequently  is  accompanied  by  palpita- 
tion, dyspnea,  and  a  rapid  pulse  of  high  tension. 


439 

The  murmur  of  aortic  stenosis  is  sometimes  audible  at  the  apex, 
as  well  as  at  its  punctum  maximum  at  the  aortic  cartilage.  But 
such  a  murmur,  though  timed  like  that  of  mitral  regurgitation, 
usually  has  a  harsh,  rough  tone  clearly  conducted  into  the  carotids, 
and  is  accompanied  by  a  basic  thrill,  by  obliteration  of  the  aortic 
second  sound,  and,  not  uncommonly,  by  a  pulsus  tardus  or  a  pulsus 
bisferiens. 

The  distinctions  between  tricuspid  regurgitation  and  a  corre- 
sponding mitral  defect  are  considered  elsewhere.  (See  p.  389.) 

MITRAL  STENOSIS 

Clinical  Pathology. — Rheumatic  endocarditis  is  unquestionably 
the  most  important  factor  of  this  variety  of  valvular  disease,  which 
ordinarily  depends  upon  an  insidious  and  progressive  valvulitis, 
arising,  in  childhood,  in  connection  with  vague  arthritic  symptoms, 
and  being  first  recognized  during  the  second  or  third  decade  of 
life  in  those  who,  as  young  children,  suffered  from  "  growing  pains  " 
and  other  atypical  manifestations  of  subacute  or  masked  rheumatism. 
Less  frequently  mitral  stenosis  is  traceable  to  an  acute  attack  of 
rheumatic  fever  attended  by  well-defined  endocarditis,  and  very 
exceptionally  the  lesion  is  to  be  regarded  as  congenital,  being  due  in 
such  instances  either  to  fetal  endocarditis  or  to  developmental  defect. 
Chorea  is  also  a  prominent  cause  of  mitral  valvulitis  and  narrowing, 
and  the  valvular  irritation  consequent  to  anemia  and  chlorosis,  as 
well  as  the  undue  stress  upon  the  mitral  leaflets  imposed  by  attacks 
of  pertussis,  may  excite  fibroid  constriction  of  the  mitral  orifice. 
Pure  mitral  stenosis  is  a  disease  of  children  and  young  adults,  rather 
than  of  advanced  life,  and  is  much  commoner  in  females  than  in  males, 
the  former  fact  being  generally  attributed  to  the  prevalence  of  rheu- 
matism in  the  young,  and  the  latter  to  the  susceptibility  of  girls 
to  rheumatism,  chorea,  and  anemia.  Persons  of  middle  or  advanced 
age  occasionally  acquire  mitral  stenosis  of  a  sclerotic  type,  under 
which  circumstances  the  lesion  is  but  part  of  a  general  arterio- 
sclerosis, and  is  commonly  associated  with  chronic  renal  disease, 
gout,  or  syphilis.  Rokitansky's  theory  that  mitral  stenosis  and 
pulmonary  tuberculosis  are  antagonistic  is  generally  regarded  as 
tenable.  The  view  that  tuberculosis  is  an  exciting  cause  of  mitral 
obstruction,  especially  of  those  types  characterized  by  slow  develop- 
ment and  progress,  is  supported  by  Potain  and  by  Tessier.  The 
association  of  mitral  stenosis  with  cholelithiasis,  which  occurs  in 
about  one-fifth  of  all  cases  of  this  type  of  valvular  disease, 
according  to  Brockbank,  has  never  been  satisfactorily  explained. 


440 


PHYSICAL   DIAGNOSIS 


The  structural  changes  in  mitral  obstruction  implicate  mainly  the 
valve  leaflets,  their  tendinous  and  muscular  attachments,  and  the 
basal  ring  of  the  orifice  (Figs.  172  and  173).  Of  the  valve  defects, 
the  two  most  distinctive  types  are  known  as  Corrigan's  "button-hole 
mitral"  and  the  so-called  "funnel-shaped  stenosis,"  of  which  the 
former  is  the  commoner  in  adults  and  the  latter,  in  children.  In  the 
button-hole  variety  of  obstruction  the  valve  segments  are  fused,  re- 
tracted, and  greatly  thickened,  with  the  result  that  the  mitral  orifice  is 


Fig.  172. — Mitral  stenosis  (Jefferson  Hospital  Laboratories). 

converted  into  a  mere  narrow  slit  or  a  somewhat  crescentic  perforation; 
in  the  funnel-shaped  stenosis  the  leaflets  are  intimately  welded  to- 
gether, and,  by  sclerotic  shortening  of  the  chordae  tendineae,  pulled 
down  into  the  cavity  of  the  left  ventricle  in  the  form  of  a  conic  structure 
the  large  orifice  of  which  points  toward  the  auricle.  In  both  these 
forms  of  obstruction  the  valve  mechanism  is  further  interfered  with 
by  more  or  less  fibrous  constriction  of  the  mitral  ring  and  by  con- 
traction and  rigidity  of  the  tendinous  cords  and  papillary  muscles, 
which,  in  extreme  instances,  appear  to  be  attached  directly  to  the 
valve  leaflets,  so  striking  is  the  shrinkage  of  the  thickened  cords. 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM 


441 


In  some  instances,  particularly  those  of  congenital  type,  stricture 
of  the  orifice  by  contraction  of  the  sclerotic  and  calcified  basal  ring, 
with  little  or  no  deformity  of  the  leaflets,  is  the  conspicuous  change. 
In  other  cases  the  orifice  is  obstructed  by  vegetations  situated  upon 
the  auricular  surfaces  of  the  leaflets  just  back  of  their  free  borders; 
the  constriction  may  be  due  to  irregular  deformities  of  the  cusps, 
depending  upon  fibrous  contraction  and  the  deposit  of  lime-salts;  or, 
rarely,  a  calcareous  plate  projects  from  the  basal  ring  into  the  lumen 


Stenotic  mitral 
orifice 


Fig.  173. — Mitral  stenosis  (Jefferson  Hospital  Laboratories). 

of  the  orifice.  Ewart  mentions  pedunculated  thrombus  attached 
to  the  left  auricular  wall  as  a  cause  of  mitral  obstruction,  and  he  has 
also  described  a  narrowing  of  the  mitral  orifice  due  to  yielding  non- 
indurative  fibrosis,  in  which  type  of  so-called  "  soft-valve  stenosis  " 
a  murmur  may  never  develop,  owing,  Ewart  maintains,  to  the  re- 
markable pliability  of  the  valve  mechanism. 

A  condition  of  relative  mitral  stenosis  is  said  to  exist  when  dilatation 
of  the  left  ventricle  is  associated  with  no  deviation  from  the  normal 


442  PHYSICAL    DIAGNOSIS 

diameter  of  the  auriculoventricular  orifice.  As  a  rule,  left  ventricular 
distention  causes  corresponding  dilatation  of  the  mitral  ring,  and 
hence  relative  mitral  incompetence  ensues,  but  should  the  ring  fail 
to  stretch,  the  orifice  necessarily  must  be  stenosed  relatively  to  the 
inordinately  large  ventricular  chamber  beyond. 

The  immediate  effects  of  mitral  stenosis  are  felt  by  the  left  auricle, 
whose  walls  hypertrophy  to  a  degree  proportionate  to  the  increased 
force  the  auricle  must  exert  to  drive  the  blood  through  the  narrowed 
outlet  into  the  ventricle.  This  primary  auricular  hypertrophy  may 
ensure  a  satisfactory  blood-supply  to  the  left  ventricle  for  a  time,  but 
usually  not  for  a  long  period,  as  the  auricle,  having  but  indifferent 
muscular  power,  tends  soon  to  dilate  under  the  undue  stress,  in 
some  instances  enlarging  to  a  most  extraordinary  degree — even  to 
twice  or  thrice  its  normal  capacity.  In  fully  50  per  cent,  of  mitral 
stenoses  the  advanced  myocardial  degeneration  attendant  thereto 
ultimately  causes  auricular  fibrillation,  in  which  these  chambers 
are  maintained  in  wide  diastole  with  their  musculature  incessantly 
quivering  with  fine  fibrillary  twitching  movements,  due  to  the  in- 
dependent origin  of  new  impulses  in  many  small  areas,  but  never 
actually  contracting  through  stimuli  sent  from  the  sino-auricular 
node  (v.  s.).  Osier  has  shown  that  the  dilated  auricle  may 
compress  the  left  recurrent  laryngeal  nerve,  exciting  a  group 
of  pressure  symptoms  like  those  attending  thoracic  aneurism. 
(See  p.  489.)  This  primary  hypertrophy  and  secondary  dila- 
tation of  the  left  auricle  hi  mitral  stenosis  stand  in  strong  con- 
trast to  the  primary  dilatation  and  secondary  hypertrophy 
of  this  chamber  in  mitral  regurgitation.  When  the  left  auricle 
fails,  the  pulmonary  congestion  consecutive  thereto  augments  the 
work  of  the  right  ventricle,  and  this  chamber  now  hypertrophies 
and  then  dilates,  in  its  effort  to  overcome  the  stasis  of  the  lesser  blood 
circuit.  This  is  unquestionably  beneficial,  in  that  the  force  of  the 
hypertrophied  ventricle  is  transmitted  through  the  pulmonary 
circulation  into  the  left  auricle,  raising  the  pressure  therein,  and 
thus  aiding  the  feeble  auricular  contractions  to  drive  the  blood 
column  onward  through  the  stenosed  mitral  orifice.  When  finally 
the  right  ventricle  fails,  relative  incompetence  of  the  tricuspid  valve 
is  inevitable,  and  ultimately  the  right  auricle,  after  a  period  of  com- 
pensatory hypertrophy,  dilates,  with  the  disastrous  consequences  refer- 
able to  general  venous  congestion.  (Seep.  432.)  In  pure  compensated 
mitral  stenosis  the  left  ventricle,  having  less  work  than  normal  to 
perform,  not  only  does  not  enlarge,  but  ordinarily  diminishes  in  size, 
becoming  atrophied,  thin  walled,  and  flabby,  and  appearing  dwarfed 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  443 

in  comparison  with  the  decidedly  hypertrophied  right  ventricle.  Left 
ventricular  atrophy,  then,  is  the  familiar  autopsy  finding  in  uncom- 
plicated mitral  stenosis,  notwithstanding  the  contention  of  some 
authors  that  the  wall  of  the  ventricle  overdevelops  in  consequence 
of  its  undue  efforts  in  performing  diastolic  aspiration  of  the  auricular 
blood,  with  which  act  an  obstructed  mitral  orifice  interferes.  When, 
however,  compensation  breaks  and  venous  stasis  is  persistent  and 
excessive,  systemic  arterial  hypertension  is  thereby  set  up,  and  to 
overcome  this  resistance  the  left  ventricle  commensurately  hyper- 
trophies. It  also  does  so,  irrespective  of  broken  compensation, 
in  that  class  of  cases  in  which  persistent  high  tension  accompanies 
the  mitral  defect.  (See  p.  410.)  Left  ventricular  hypertrophy 
naturally  attends  double  mitral  lesions,  as  the  result  of  the  regurgi- 
tation. 

Physical  Signs. — Inspection. — Interference  with  the  pulmonary 
circulation  accounts  for  the  chief  objective  evidences  of  mitral  stenosis 
• — early,  persistent,  and  increasing  dyspnea;  cough  productive  of 
liquid,  and  frequently  hemorrhagic,  sputum;  and  cyanosis  varying 
in  degree  from  a  slight  dusky  flush  upon  the  cheeks  to  intense  diffuse 
blueness  of  the  face  and  extremities.  Striking  pallor  of  the  skin 
and  blanching  of  the  mucous  membranes,  with  other  evidences  of 
well-marked  anemia  and  its  consequences,  are  frequently  seen  in 
women  who  suffer  from  mitral  stenosis.  As  a  rule,  edema  is  not  so 
conspicuous  as  it  is  in  mitral  regurgitation,  though  it  occurs,  of 
course,  when  right  heart  failure  leads  to  general  venous  stasis. 
Clubbing  of  the  finger-tips,  and,  in  children,  unnatural  promi- 
nence of  the  lower  sternal  area,  are  familiar  signs  in  cases  of  long 
standing. 

Systolic  throbbing  is  visible  in  the  epigastrium  and  lower  part  of  the 
sternum  when  the  right  ventricle  is  considerably  hypertrophied,  and 
the  impact  of  this  chamber's  conus  arteriosus  is  occasionally  percep- 
tible, in  thin-chested  subjects,  at  the  left  of  the  sternum  in  the  fourth, 
the  third,  or,  rarely,  the  second  interspace.  Systolic  jugular  pulsation 
is  noticeable  when  secondary  tricuspid  leakage  is  well  established. 
The  apex-beat,  if  strong  enough  to  be  seen,  is  found  to  occupy  an 
approximately  normal  position. 

Palpation. — In  well-compensated  mitral  obstruction  palpation  at 
or  just  above  the  apex  detects,  with  great  constancy,  a  rough  pre- 
systolic  thrill  occupying  either  the  latter  part  or  the  whole  of  the 
diastolic  period,  and  terminating  in  a  short,  sharp  ventricular  shock. 
Sometimes  the  thrill  is  not  unlike  the  soft  purring  of  a  cat — hence  the 
term,  "fremissement  cataire"  of  the  French  school;  and,  as  a  rule, 


444  PHYSICAL   DIAGNOSIS       . 

it  is  circumscribed  to  the  neighborhood  of  the  apex,  and  is  intensified 
during  expiration,  by  active  exercise,  and  by  left  lateral  decubitus. 
The  discovery  of  this  dual  sign — presystolic  thrill  and  systolic 
shock — is  of  itself  proof  positive  of  mitral  stenosis.  Other  tactile 
signs  to  be  noted  in  this  lesion  include  a  sharp  impact  in  the  pulmonic 
area,  caused  by  the  sudden  closure  of  the  pulmonic  valve,  and  also 
the  right  ventricular  pulsations  alluded  to  above. 

Preceding  the  stage  of  cardiac  breakdown  the  pidse,  though  small, 
is  of  relatively  high  tension,  and  regular  in  rhythm  and  in  frequency, 
the  artery  being  of  small  size  and  full  between  beats,  probably  in 
consequence  of  contraction  of  the  general  arterial  system  to  ensure 
its  accommodation  to  the  diminished  ventricular  output  of  blood.  A 
radial  tracing  made  at  this  period  indicates  a  wave  of  small  amplitude, 
characterized  by  an  oblique  upstroke,  a  blunt  apex,  and  a  gradually 
falling  downstroke  having  a  poorly  denned  dicrotic  notch;  later  the 
sphygmogram  shows  most  graphically  the  character  of  the  various 
irregularities  of  rate,  rhythm,  and  force  noticed  by  feeling  the  pulse 
during  the  stage  of  disturbed  compensation.  These  tracings,  how- 
ever, show  nothing  distinctive. 

Percussion. — Owing  to  the  right  ventricular  enlargement,  the  area 
of  cardiac  dulness  extends  considerably  beyond  the  right  sternal 
border,  dulling  Ebstein's  angle  and  obliterating  the  pulmonary 
resonance  for  a  considerable  distance  to  the  right  of  this  point, 
between  the  third  and  the  fifth  interspaces.  To  the.  left  of  the 
sternum  there  may  be  dulness,  generally  within  the  midclavicular 
line,  extending  from  the  second  or  third  rib  to  the  apex,  the  greater 
part  of  this  area  corresponding  to  the  site  of  the  enlarged  right 
ventricle.  In  mitral  stenosis,  with  no  hypertrophy  of  the  left 
ventricle,  the  lower  left  cardiac  limit  is  not  unnaturally  extended. 
According  to  Potain,  the  abnormally  large  left  auricle  of  a  pure  mitral 
obstruction  is  capable  of  producing  an  oblong  area  of  impaired 
resonance,  about  4^  by  z\  inches  (11.2  by  6.2  cm.)  in  extent,  in 
the  left  interscapular  region,  and  to  the  stabbing  sensation  provoked 
by  strong  percussion  over  this  area  Vasquez  has  given  the  name 
"  auricular  pain."  Enlargement  of  the  hepatic  area  supervenes  in 
the  late  stages  of  mitral  stenosis,  in  consequence  of  passive  venous 
congestion  of  the  liver. 

Auscultation. — The  auscultatory  findings  in  mitral  stenosis  differ 
very  radically  according  to  the  mechanical  conditions  prevailing 
during  the  progress  of  the  lesion,  in  view  of  which  Sir  William  H. 
Broadbent's  plan  of  grouping  the  sounds  and  murmurs  in  three 
stages  is  most  helpful  (Fig.  174).  In  the  first  stage,  that  of  ade- 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM 


445 


quate  compensation,  auscultation  at  the  apex  affords  three  dis- 
tinctive sounds:  a  rough,  rumbling  presystolic  murmur,  abruptly 
terminating  in  a  sharp,  snappy  first  sound,1  and  followed,  after  a 
prolonged  diastolic  interval,  by  a  distinct,  occasionally  reduplicated, 
second  sound.2  Rarely,  a  short  interval  separates  the  murmur 
from  the  first  sound,  a  peculiarity  which  Mackenzie  attributes  to 
delay  in  the  transmission  of  the  contraction  stimulus  between 


First  stage 


/m 


Second  stage 


Third  stage 


Murmur  Sound  Sound 

Fig.  174. — The  murmur  of  mitral  stenosis. 


auricle  and  ventricle.  At  the  base  the  pulmonic  second  sound  is 
sharply  accentuated  and  frequently  doubled,  while  the  aortic  second 
sound  either  remains  of  normal  intensity  or  is  enfeebled. 

1  The  apical  first  sound  may  be  reduplicated  (from  asynchronous  mitral  and 
tricuspid  valve  closure),  but  this  peculiarity  is  of  far  less  diagnostic  moment 
than  the  sharp  snappiness  of  the  sound. 

2  This  reduplication  of  the  second  sound  at  the  apex  (Sansom's  "double  shock 
sound")  is  attributed  to  sudden  tension  of  the  mitral  cusps,  primarily  dependent 
upon  increased  intra-auricular  pressure,  whereby  the  blood-column  is  driven 
with  undue  velocity  into  the  ventricle.      Apical  reduplication  of  the  second 
sound,  since  it  may  precede  the  development  of  the  presystolic  murmur,  is  an 
important  early  sign  of  mitral  obstruction. 


446  PHYSICAL   DIAGNOSIS 

The  murmur  occupies  a  short  interval  immediately  before  ventric- 
ular systole,  and  is  distinguished  by  rolling,  vibratory  quality,  by  low 
pitch,  and  by  gradually  increasing  intensity,  or  ingravescence,  toward 
its  abrupt  termination.  Its  punctum  maximum  is  just  above  and 
somewhat  within  the  apex-beat,  where,  as  a  rule,  the  murmur  is 
sharply  localized,  though  in  some  instances  its  audibility  extends, 
in  the  shape  of  a  roughly  pyramidal  area,  from  midsternum  to  mid- 
axilla  (Fig.  153).  A  mitral  stenotic  murmur,  however,  is  never  trans- 
mitted, in  the  ordinary  sense  of  the  word.  Although  generally 
ascribed  to  blood  eddies  created  by  the  auricular  contraction,  there 
is  also  truth  in  Colbeck's  belief  that  the  bruit  of  mitral  stenosis  like- 
wise may  be  due  to  vibrations  excited  in  the  long  anterior  mitral  flap 
by  the  impact  of  the  auricular  blood  stream. 

Inconstancy  and  variation  in  intensity  and  duration  are  other 
peculiarities  of  this  murmur,  which  is  prone  to  appear  and  to  dis- 
appear erratically  in  the  same  patient,  and  to  become  soft  and  in- 
distinct and  prolonged  when  the  heart  is  beating  rapidly.  The  sharp 
snappiness  of  the  apical  first  sound  corresponds  to  the  systolic  shock 
felt  at  the  apex,  and  though  both  phenomena  are  obviously  due  to 
a  common  cause,  their  precise  nature  is  a  matter  of  much  contro- 
versy; perhaps  the  best  explanation  assumes  an  incomplete  filling  of 
the  left  ventricle,  whereby  the  contraction  of  the  muscular  wall,  at 
first  unopposed,  is  suddenly  arrested  by  contact  with  the  contained 
blood  before  the  completion  of  systole. 

The  second  stage,  characterized  by  beginning  failure  of  the  left 
auricle  and  by  hypertension  of  the  pulmonary  circuit,  is  accompanied 
by  certain  alterations  in  the  character  of  the  murmur,  by  increased 
intensity  of  the  first  sound,  and  by  disappearance  of  the  second 
sound  at  the  apex.  The  murmur,  hitherto  a  short  continuous 
crescendo  just  before  systole,  now  tends  to  become  prolonged  and 
wavy  or  actually  interrupted.  In  other  words,  it  now  corresponds 
not  only  to  the  time  of  the  auricular  systole,  but  also  to  the  time  of 
the  ventricular  diastole,  which  creates  a  suction  force  at  the  mitral 
orifice  sufficient  to  generate  an  additional  sound  during  the  early 
part  of  the  diastolic  period.  It  is  this  suction  murmur,  due  to  the 
diastolic  recoil  of  the  left  ventricle,  that  accounts  for  the  sound  now 
audible  at  the  beginning  of  diastole,  before  the  appearance  of  the 
strictly  presystolic  bruit  produced  by  the  auricular  force.  The 
murmur  audible  at  this  stage  may  occupy  the  entire  diastolic  period, 
beginning  immediately  after  the  second  sound  and  continuing  up  to 
the  sharp  first  sound,  as  a  continuous  bruit  having:  (a)  a  mid-diastolic 
diminuendo  and  a  presystolic  crescendo;  or  (ft)  a  double  crescendo 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM  447 

wave;  or  (c)  a  mid-diastolic  crescendo  and  a  presystolic  diminuendo. 
Should  the  ventricular  suction-action  be  expended  before  the  auric- 
ular contraction-force  begins,  the  murmur  will  be  actually  inter- 
rupted at  about  the  middle  of  diastole,  so  that  it  consists  of  two 
separate  phases — one  audible  immediately  after  diastole  and  the 
other  immediately  before  systole.  Should  the  auricular  force  fail, 
but  the  ventricular  suction  persist,  the  strictly  presystolic  rumble 
will  be  suppressed,  in  which  case  but  a  single  short  sound,  at  the 
very  beginning  of  the  diastolic  period,  is  detected.  Should  the 
pressure  within  the  ventricle  fall  below  that  within  the  auricle,  the 
characteristic  presystolic  rumble  is  replaced  by  a  much  softer 
diastolic  diminuendo  murmur  generated  at  the  narrow  mitral 
orifice  at  the  moment  its  valves  open.  In  the  event  of  auricular 
fibrillation,  with  the  abolition  of  every  vestige  of  the  auricular 
contraction  force,  this  diastolic  murmur  is  commonly  followed  by 
a  distinct  period  of  silence  just  before  systole,  the  adventitious 
sound  being  ascribed  to  the  increased  velocity  of  the  blood  flow 
during  early  diastole  and  the  succeeding  silence  to  the  slow- 
ing of  the  current  during  late  diastole.  In  general,  Dagnini's 
statement  is  true,  that  early  and  mid-diastolic  murmurs  are 
more  frequent  in  double  mitral  lesions  than  in  pure  stenosis. 
Aside  from  the  changes  in  the  murmur,  the  increased  loudness  and 
sharpness  of  the  apical  first  sound  and  the  disappearance  of  the 
second  sound  at  the  apex  are  clinically  important  signs.  Maintain- 
ing that  the  second  sound  audible  at  the  apex  is  the  transmitted 
aortic  (not  pulmonic)  tone,  its  disappearance  in  mitral  stenosis  is 
commonly  attributed  to  two  factors:  first,  weakening  of  the  aortic 
second  sound  by  the  diminished  tension  of  the  aortic  cusps  consequent 
to  the  restricted  output  of  blood  by  the  left  ventricle;  and,  second, 
non-transmission  of  this  enfeebled  aortic  second  sound  to  the  pre- 
cordia,  owing  to  the  backward  displacement  of  the  left  ventricle  by 
the  hypertrophied  and  dilated  right  heart.  Corresponding  enfeeble- 
ment  of  the  second  sound  in  the  aortic  area,  and  accentuation, 
generally  also  reduplication,  of  the  second  sound  in  the  pulmonic 
area  are  corroborative  of  the  foregoing  explanation. 

The  third  stage  is  distinguished  by  striking  enfeeblement  or  even 
total  disappearance  of  the  presystolic  murmur,  and  when  this 
happens,  the  short,  sharp  first  sound  is  the  sole  auscultatory 
sign  distinguishable  at  the  apex,  since  already  the  apical  second 
sound  has  been  effaced.  Comcidentally,  the  accentuation  of 
the  pulmonic  second  sound  at  the  base  disappears,  and  its  aortic 
equivalent  becomes  still  weaker.  This  stage  of  the  lesion  corre- 


448  PHYSICAL  DIAGNOSIS 

spends  to  extreme  dilatation  of  the  left  auricle  and  the  right  ven- 
tricle, and  to  auricular  fibrillation,  with  the  establishment  of  tricus- 
pid  leakage  and,  in  consequence,  lowering  of  the  pressure  within  the 
pulmonary  circuit  and  the  left  auricle.  The  force  of  the  auricular 
contractions  is  now  so  lessened  and  the  tension  within  the  auricle  is 
at  so  low  an  ebb  that  a  murmur  is  no  longer  generated.  However, 
should  the  heart  regain  its  tone,  as  is  not  infrequently  the  case,  the 
murmur  may  reappear,  its  persistence  depending  upon  the  mechanical 
forces  active  at  different  periods.  In  addition  to  the  presystolic 
murmur,  the  majority  of  mitral  stenoses  also  afford  the  systolic  bruit 
of  mitral  regurgitation,  and,  during  the  advanced  stage,  a.  similar 
sound  referable  to  secondary  tricuspid  leakage.  Sometimes  it  is 
also  possible  to  recognize  the  so-called  "murmur  of  high  pressure," 
indicative  of  relative  pulmonary  leakage.  (See  Relative  Pulmonary 
Regurgitation,  p.  473.) 

Diagnosis. — A  rough  presystolic  murmur  and  thrill,  with  a  snappy 
first  sound  and  a  reduplicated  second  sound  at  the  apex,  are  character- 
istic of  mitral  stenosis.  Restriction  of  the  murmur  and  thrill  to  the 
apical  region  and  their  ingravescent  quality,  accentuation  of  the  pul- 
monic  second  sound  at  the  base,  enlargement  of  the  right  ventricle 
rather  than  of  the  left,  and  a  small  thready  pulse  are  corroborative  evi- 
dence not  to  be  overlooked.  Later,  as  the  murmur  and  the  second 
sound  become  indistinct  and  evanescent  at  the  apex,  the  character  of 
the  other  heart-sounds  are  the  most  definite  guides.  As  the  power  of 
the  heart  wanes,  the  pulmonic  second  sound,  for  a  long  period  accen- 
tuated, finally  weakens  at  the  base;  and  the  aortic  second  sound, 
already  lost  at  the  apex,  becomes  almost  inaudible  in  the  aortic  area; 
but  despite  all  this,  the  first  sound  still  snaps  sharply  at  the  apex. 
This  sign,  interpreted  in  the  light  of  other  clinical  information,  may 
be  sufficient  to  warrant  a  diagnosis  of  mitral  obstruction  during  the 
stage  of  broken  compensation. 

Discrimination  between  the  Flint  murmur  of  aortic  regurgitation 
and  the  bruit  of  organic  mitral  constriction  must  sometimes  be  equivo- 
cal, for  both  are  similarly  timed,  have  a  common  punctum  maximum, 
are  restricted  to  the  apex,  and  may  be  accompanied  by  the  same 
sort  of  thrill.  In  a  given  case  of  Corrigan's  disease  with  a  basic 
diastolic  and  an  apical  presystolic  murmur,  the  latter  probably 
represents  a  spurious  obstruction,  if  unattended  by  a  systolic  shock, 
a  snappy  first  sound,  an  accentuated  pulmonic  second  sound,  and 
enlargement  of  the  right  ventricle.  Moreover,  a  Flint  murmur 
generally  is  less  intense,  rumbling,  and  ingravescent  than  the  bruit 
of  true  stenosis,  while  the  pulse  does  not  become  small  and  thready, 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM  449 

but  retains  its  collapsing  character.  Syllaba  advises,  in  studying 
doubtful  cases,  the  use  of  digitalis,  the  action  of  which  quiets  or 
dissipates  the  murmur  of  Flint. 

Tricuspid  stenosis,  though  almost  unique  as  an  isolated  lesion, 
must  not  be  overlooked  as  a  possible  counterfeit  of  mitral  obstruction, 
for  a  circumscribed  presystolic  thrill  and  murmur,  with  a  sharp 
first  sound,  are  common  to  both.  These  signs,  restricted  to  the 
tricuspid  area  and  attended  by  right  auricular  dilatation  and  venous 
congestion  without  pulmonary  engorgement,  warrant  the  diagnosis 
of  tricuspid  obstruction.  In  doubtful  cases  it  is  helpful  to  remember 
that  in  this  affection,  owing  to  the  relatively  weak  contractions  of  the 
right  auricle,  the  murmur  is  likely  to  be  lower  and  less  rumbling, 
while  the  tactile  vibrations  are  less  distinct  than  in  its  mitral  counter- 
part; and  also  that,  exceptionally,  the  liver  shows  presystolic  (auricu- 
lar) pulsation.  When  mitral  and  tricuspid  stenosis  coexist  the  signs 
of  the  former  usually  so  completely  overshadow  those  of  the  latter 
that  the  right-sided  defect  escapes  attention.  When  the  tricuspid 
signs  are  well  denned,  one  sometimes  detects  two  thrills  and  two 
murmurs  of  virtually  identical  nature,  save,  perhaps,  for  differences 
in  quality  and  pitch,  and  for  the  important  fact  that  one  is  localized 
at  the  cardiac  apex  and  the  other  at  the  base  of  the  ensiform, 
between  which  puncta  maxima  lies  a  silent  area  over  which  neither 
bruit  can  be  heard.  Cyanosis,  dropsy,  and  other  evidences  of 
venous  obstruction  are  no  criteria  in  distinguishing  right-  and 
left-sided  auriculoventricular  stenoses,  nor  is  the  character  of  the 
pulse  a  guide. 

Pericarditis  in  children  is  occasionally  followed  by  the  development 
of  a  rumbling  presystolic  apical  murmur,  which  Broadbent  believes 
is  "possibly  a  result  of  pericardial  adhesions."  This  murmur, 
unlike  that  of  true  mitral  stenosis,  lacks  a  vibratory,  crescendo 
character,  and  does  not  terminate  abruptly  in  a  snappy  first  sound; 
while  the  exocardial  origin  of  such  a  bruit  is  suggested  by  its  appear- 
ance after  an  attack  of  pericarditis  and  by  its  association  with  other 
physical  signs  thereof. 


AORTIC  REGURGITATION 

Clinical  Pathology. — This  dangerous  type  of  heart  disease  was 
first  established  as  a  clinical  entity  in  1832  by  the  brilliant  Irish 
physician,  Sir  Dominick  Corrigan,  who  termed  the  lesion  a  "  perma- 
nent patency  of  the  mouth  of  the  aorta."  Ordinarily,  it  affects 

men  of  middle  age,  and  is  the  consequence  of  a  gradual,  progressive 
29 


450 


PHYSICAL   DIAGNOSIS 


sclerosis,  of  which  unremitting  muscular  strain,  alcohol,  and  syphi- 
lis, combined  or  singly,  are  the  material  factors;  to  some  degree  it 
is  probable  that  plumbism  and  gout  have  a  similar  influence.  The 
essential  cause,  then,  of  this  type  of  heart  disease  consists  of  long- 
continued  irritation  of  the  aortic  cusps,  both  by  their  exposure  to 
excessive  tension  during  diastole  and  by  the  action  of  circulatory 
poisons.  This  being  so,  it  is  easy  to  understand  the  predilec- 


Aortic  orifice 


Fig.  175. — Aortic   regurgitation   and   double   mitral   lesion.     Aortic   and   auricular 
aspects  (Jefferson  Hospital  Laboratories). 

tion  of  aortic  leakage  for  sailors,  soldiers,  stevedores,  stokers,  and 
other  men  whose  occupations  entail  habitual  muscular  strain  and 
whose  tastes  perchance  run  to  alcohol  and  to  venery.  "Athlete's 
heart"  and  "jinrikisha  heart"  are  medical  slang  for  the  aortic 
regurgitation  occurring  in  the  athlete,  and  in  the  rickshaw  man  of  the 
Orient.  Less  commonly  the  aortic  leaflets  are  damaged  by  endocar- 
ditis, whereby  valvular  induration,  puckering,  and  adhesion,  together 
with  vegetation,  erosion,  and  dense  fibrocalcareous  deformity,  are  the 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM  451 

various  lesions  provoked,  according  to  the  extent  and  malignancy  of 
the  inflammation.  In  regurgitation  of  endocarditic  origin  it  is  also 
true  that  males  are  more  predisposed  than  females,  but  here  middle 
age  is  not  a  prominent  etiologic  factor.  Traumatic  aortic  regurgita- 
tion, from  rupture  of  a  leaflet,  though  very  rare,  occasionally  follows 
a  sudden  violent  strain;  it  is  hard  to  believe  that  this  accident  can 
happen  so  long  as  the  valve  is  normally  resistant,  though  when 
damaged  by  sclerosis  or  erosion,  a  cusp  is  not  unlikely  to  be  torn  or 
perforated  under  the  stress  of  great  muscular  exertion  or  even  by 
inordinate  arterial  hypertension.  Exceptionally,  the  aortic  orifice 
leaks  because  the  valve  is  congenitally  malformed,  and  in  such 
instances  it  is  usual  to  find  sclerotic  valvulitis  with  fusion  of  two  cusp 
borders,  and  hence,  conversion  of  the  valvular  apparatus  into  a  double 
instead  of  a  triple  set  of  leaflets.  Aortic  regurgitation,  whether 
sclerotic  or  endocarditic,  is  commonly  attended  by  more  or  less 
stenosis,  owing  to  the  frequent  coincidence  of  fibrous  contraction 
at  the  aortic  ring  sufficient  to  obstruct  the  systemic  blood-column 
passing  through  this  aperture.  The  systemic  arteries  do  not  often 
escape  fibrosis,  owing  to  the  circulatory  wear  and  tear  provoked 
by  the  powerful  ventricular  contractions,  which,  despite  their  force, 
are  not  always  able  properly  to  fill  the  arteries,  if  the  aortic  reflux 
be  excessive.  The  circulation  within  the  coronary  arteries  is  greatly 
disturbed,  and  these  vessels  are  damaged  by  sclerotic  degeneration — 
defects  leading  to  muscular  degeneration  of  the  heart.  In  many 
instances  the  first  part  of  the  aorta  is  the  seat  of  fibrosis,  atheroma, 
and  calcification,  whereby  permanent  dilatation  is  favored.  So-called 
"dynamic  dilatation"  of  the  aortic  arch,  simulating  the  physical 
signs  of  aneurism  and  occasionally  met  with  in  Corrigan's  dis- 
ease, is  due  merely  to  the  violent  systolic  shocks  of  the  voluminous 
blood-columns  within  a  resilient  and  distensible  aorta,  having  no 
actual  enlargement  of  its  caliber  and  no  traces  of  mural  disease. 

Aside  from  the  foregoing  types  of  aortic  reflux,  essentially  referable 
to  valvular  deformity,  regurgitation  also  occurs  into  the  ventricle 
when  the  aortic  ring  and  the  ventricular  wall  are  so  stretched  that  the 
leaflets  of  the  valve  fail  to  approximate  during  diastole.  This 
so-called  relative  aortic  incompetence  is  much  less  common  than  a 
corresponding  leakage  at  the  mitral  orifice,  since  the  aortic  ring, 
being  stouter  and  denser,  does  not  readily  enlarge  to  a  caliber  render- 
ing perfect  coaptation  of  its  valve  cusps  impossible.  Relative  aortic 
incompetence  follows  stretching  of  the  aortic  ring  secondary  to 
myocardial  degeneration,  atheromatous  dilatation  of  the  aortic  root, 
aneurism  of  the  ascending  arch  of  the  aorta,  and  pressure  stenosis 
of  this  vessel. 


452 


PHYSICAL   DIAGNOSIS 


In  aortic  regurgitation  the  left  ventricle  bears  the  brunt  of  the 
damage,  since  with  diastole  this  chamber  receives  not  only  its  normal 
quota  of  blood  from  the  auricle,  but  also  the  stream  regurgitated 
from  the  aorta  through  the  leaky  semilunar  cusps.  Surcharged  in 
this  manner,  the  ventricle  dilates  in  order  to  accommodate  the  undue 
blood  volume,  and  hypertrophies  so  as  adequately  to  propel  its 
contents  aortaward.  This  habitual  overwork  in  time  creates  that 
extreme  grade  of  eccentric  hypertrophy  of  the  left  ventricle  termed 
cor  bovinum,  or  ox  heart,  the  weight  of  which  may  be  three  or  even 
four  times  that  of  the  normal  organ  (Fig.  164).  So  long  as  this  conserv- 
ative hypertrophy  predominates,  the  valvular  lesion  is  compensated 
by  the  increased  ventricular  output  thereby  made  possible,  but  inevit- 
ably dilatation  gains  the  upper  hand,  owing  to  the  pernicious  action 
of  the  persistent  ventricular  overdistention  and  to  myocardial  mal- 
nutrition due  to  defective  coronary  blood-supply.  When,  finally,  the 
ventricle  gives  way  and  no  longer  can  pump  sufficient  blood  into  the 


Aortic 


Diastole 
Fig.  176. — Mechanism  of  the  murmur  of  aortic  regurgitation. 

systemic  circuit  to  satisfy  its  demands,  failure  of  compensation  super- 
venes. Relative  leakage  at  the  auriculoventricular  orifice  occurs  with 
systole,  because  of  the  strain  upon  the  mitral  ring,  if,  indeed,  the 
valve's  integrity  is  not  already  impaired  by  pathologic  changes,  and 
in  consequence  of  this  incompetence  a  wave  of  backward  pressure  is 
transmitted  into  the  left  auricle,  the  pulmonary  veins,  and  the  right 
heart,  with  the  baneful  effects  already  recounted  in  connection  with 
mitral  regurgitation.  (See  p.  435.) 

Physical  Signs. — Inspection. — Violent  arterial  throbbing  is  a 
noteworthy  sign  of  Corrigan's  disease,  and  in  some  instances  one  is 
almost  justified  in  hazarding  the  diagnosis  by  this  evidence  alone. 
The  pulsations,  systolic  in  time  and  perhaps  so  vigorous  as  to  jog  the 
patient's  head  with  every  heart-beat  (Mussefs  sign) ,  are  particularly 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  453 

conspicuous  in  the  carotid  and  subclavian  arteries  of  the  neck,  in 
the  temporals  of  the  face,  and  in  the  brachials  of  the  arm,  while  in 
the  episternal  notch  an  aortic  throb  is  generally  visible.  Even  the 
small  arteries,  such  as  the  radial  and  the  dorsalis  pedis,  may  pulsate 
visibly,  showing  in  miniature  the  powerful  beats  of  the  larger  arterial 
trunks.  If  tortuous,  a  superficial  artery,  such  as  the  brachial,  may 
not  only  pulsate,  but  even  become  displaced  and  elongated  with 
every  beat — the  locomotive  or  movable  pulse.  Penetration  of  the 
capillaries  by  the  pulse-wave  produces  pulsation  of  these  small 
vessels,  to  which  the  term  capillary  pulse  is  applied  (see  p.  345) ; 
and,  rarely,  the  superficial  veins,  notably  those  of  the  hand  and 
forearm,  show  postsystolic  undulations  created  by  arterial  waves 
of  sufficient  force  to  penetrate  the  delicate  venous  radicles — the 
penetrating,  direct,  or  centripetal  venous  pulse.  (See  p.  349.)  Pulsa- 
tion and  tortuosity  of  the  retinal  arteries  are  sometimes  visible  with 
the  ophthalmoscope.  The  precordial  area  heaves  under  the  impact 
of  the  enlarged  heart,  and,  in  the  case  of  a  thin-walled,  resilient 
thorax,  it  may  show  unnatural  protrusion.  A  violent  pulse  in  the 
abdominal  aorta  causes  an  epigastric  throb.  The  apical  impulse 
appears  extraordinarily  broad  and  powerful,  and  .is  displaced  from 
one  to  three  interspaces  downward  and  outward  toward,  if  not, 
indeed,  as  far  as,  the  left  anterior  axillary  line.  In  certain  subjects 
atmospheric  pressure  produces  a  circumscribed  systolic  recession  of  the 
third  and  fourth  interspaces  between  the  left  sternal  and  midclavicular 
lines,  and  in  such  instances  a  systolic  thrill  at  the  apex  may  be  very 
closely  counterfeited  by  costal  vibrations  set  up  by  the  violent  and 
sharp  cardiac  impulse.  These  remarks  apply  to  a  well- developed 
example  of  aortic  regurgitation  with  decided  left  ventricular  hyper- 
trophy, considerable  reflux  from  the  aorta,  and  marked  arterial 
relaxation,  but  when  such  conditions  do  not  obtain,  it  is  obvious  that 
suitable  modifications  of  these  visual  signs  are  to  be  made.  Pallor 
of  the  skin  and  mucous  membranes  is  a  common  sign  in  aortic 
regurgitation,  especially  during  the  advanced  stages,  and,  when 
compensation  fails,  cyanosis,  dyspnea,  cough,  edema,  and  other 
evidences  of  venous  obstruction  supervene.  Ague-like  attacks  not 
infrequently  light  up  from  time  to  time  as  a  symptom  of  recurrent 
endocardial  inflammation. 

Palpation. — A  heaving,  tumultuous,  lifting  impulse  of  wide  extent 
is  perceived  by  laying  the  palm  of  the  hand  upon  the  precordia,  but 
later,  as  dilatation  predominates,  this  sign  of  ventricular  hypertrophy 
is  replaced  by  a  feebler,  less  extensive,  and  somewhat  undulatory 
pulsation.  Occasionally  there  is  a  prolonged  diastolic  thrill  at 


454  PHYSICAL   DIAGNOSIS 

the  base  of  the  heart,  due  to  vibrations  excited  by  the  regurgitant 
blood-column;  a  systolic  thrill  in  the  episternal  notch,  if  the  aorta 
be  greatly  dilated;  and  a  presystolic  thrill  near  the  apex,  suggestive 
either  of  a  Flint  murmur  or  of  a  true  mitral  stenosis  (v.  i.) .  Rarely 
a  distinct  thrill  may  be  felt  over  one  of  the  smaller  arteries,  such  as 
the  brachial.  A  short,  sharp  diastolic  impact  in  the  region  of  the 
apex  suggests  sudden  recoil  of  the  left  ventricle  under  the  burden  of  a 
large  volume  of  reflux  blood.  Rarely,  it  is  possible  to  distinguish 
arterial  pulsation  over  the  liver,  and,  very  exceptionally,  over  the 
spleen.  One  obtains  a  good  idea  of  the  general  arterial  overaction 
by  grasping,  with  firm  compression,  the  subject's  arm  just  above  the 
elbow,  so  as  to  obstruct  the  circulation  and  create  an  exaggerated 
distensive  pulsation  proximal  to  the  constriction.  (Beardsley.) 

The  ptilse  is  very  characteristic  in  most  cases  of  aortic  regurgitation; 
it  is  commonly  known  as  the  "Corrigan  pulse,"  owing  to  its  lucid 
description  by  Corrigan,  but  is  also  termed  the  "pulsus  altus  et  celer," 
the"pulsuscelerrimus,"  the  "water-hammer  pulse,"  the  " collapsing 
pulse,"  the  "receding  pulse,"  and  the  "pistol  pulse."  In  the  radial 
arteries  the  pulse-wave  rises  suddenly  and  with  extraordinary  force, 
strikes  the  palpating  finger  with  a  momentary  shot-like  impact,  and 
then  instantly  collapses,  the  strong  impact  representing  the  concussion 
of  the  large  column  of  blood  hurled  aorta  ward  by  the  hypertrophied 
left  ventricle,  and  the  quick  collapse  indicating  the  rapid  depletion 
of  the  arteries  due  to  diastolic  reflux  of  the  blood-column  through 
the  leaky  aortic  valve  into  the  left  ventricle.  The  Corrigan  pulse, 
particularly  its  collapsing  character,  is  exaggerated  by  raising  the 
subject's  arm  vertically  above  the  head,  so  as  to  take  advantage  of 
the  force  of  gravity;  its  peculiarities  are  masked  by  arterial  sclerosis 
of  a  grade  sufficient  to  impair  the  resiliency  of  the  vessels  and  hence 
their  ability  to  carry  an  undue  volume  of  blood.  Dilatation  of  the 
left  ventricle  with  mitral  insufficiency  also  negatives  this  pulse,  by 
weakening  the  ventricular  systole  and  diminishing  (he  output  of 
blood.  As  the  cardiac  strength  wanes  the  pulse  quickens,  weakens, 
and  becomes  irregular  in  time  and  in  force,  and  occasional  extra 
systoles  of  a  tired  ventricle  become  perceptible  between  the  more 
forcible  beats.  An  unduly  long  interval  between  the  apical  impulse 
and  the  radial  beat  indicates  a  prolonged  ventricular  systole. 

The  characteristic  pulse  tracing  of  aortic  leakage  indicates  great 
amplitude,  showing  a  high,  abrupt  upstroke,  a  sharp  apex  with  an 
acute  angle,  and  a  rapidly  falling  downstroke,  having  a  poorly  de- 
fined, if  not  entirely  obliterated,  dicrotic  undulation.  (See  Fig.  130, 
xni ;  p.  341.)  The  exaggerated  amplitude  and  the  sudden  rise  and 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  455 

fall  of  the  tracing,  so  distinctive  of  this  sphygmogram,  are  materially 
modified  by  myocardial  failure,  by  concomitant  mitral  incompetence, 
and  by  arteriosclerosis. 

Recent  experimental  studies  by  H.  A.  Stewart  indicate  that  aortic 
leakage  is  accompanied  by  a  fall  of  systolic  blood-pressure  presum- 
ably due  to  increased  capillary  flow.  Leonard  Hill  has  proved  that 
the  systolic  blood-pressure  of  the  leg  greatly  exceeds  that  of  the 
arm,  a  difference  of  from  50  to  100  mm.  of  Hg  being  not  unusual, 
whereas  in  health  this  difference  is  seldom  greater  than  10  mm. 
Unduly  low  diastolic  pressures  with  high  pulse-pressures  are  the 
rule  in  the  average  case. 

The  palpatory  method  of  sphygmomanometry  is  usually  pre- 
ferred to  the  auscultatory  in  aortic  regurgitation,  owing  to  the 
persistence  of  a  murmurish  tone  during  the  phases  ordinarily  occu- 
pied by  the  sharp  and  dull  sounds  preceding  and  coinciding  with 
the  diastolic  pressure  stage.  But,  despite  this  confusing  element 
of  sound,  it  is  rarely  impossible  to  identify  the  dull  tone  of  the 
minimal  pressure.  (See  p.  33.) 

Percussion. — There  is  downward  and  outward  extension  of  the 
cardiac  area,  commensurate  with  the  displacement  of  the  apex-beat 
already  noted,  and,  after  compensation  breaks,  this  area  perceptibly 
broadens,  the  left  limit  of  the  dilated  left  ventricle  extending  upward 
and  outward  and  its  apical  outline  becoming  blunt.  Ultimately, 
the  cardiac  dulness  may  encroach  well  beyond  the  right  sternal 
border,  as  secondary  enlargement  of  the  right  ventricle  progresses. 

Auscultation. — During  ventricular  diastole  a  murmur  is  audible 
at  the  base  of  the  heart  whence  it  is  transmitted,  with  variable  dis- 
tinctness, downward  over  the  precordia,  and,  exceptionally,  beyond 
this  limit  (Fig.  156).  The  murmur  is  peculiar  in  having  no  constant 
punctum  maximum  and  no  definite  line  of  propagation  common  to 
every  case,  these  two  details  of  the  sound  varying  with  the  nature  of 
the  structural  changes  predominating  in  the  individual  heart. 
The  murmur  usually  is  louder  and  more  distinct  at  about  the  middle 
of  the  sternum  at  the  level  of  the  third  rib  rather  than  at  the  tradi- 
tional aortic  cartilage,  or  it  may  be  heard  most  clearly  along  the  left 
sternal  border  at  some  point  between  the  third  rib  and  the  ensiform, 
while  exceptionally  the  punctum  maximum  is  at  the  apex.  A  sort  of 
double  punctum  maximum  is  sometimes  definable :  one  at  the  apex 
and  the  other  at  the  aortic  cartilage,  between  which  two  points  the 
bruit  is  either  quite  inaudible  or  greatly  suppressed. 

The  murmur  may  be  propagated  along  one  of  three  different  lines, 
vertically  downward  along  the  sternum  to  the  ensiform  cartilage, 
obliquely  downward  toward  the  apex,  or  horizontally  outward  toward 


456 


PHYSICAL   DIAGNOSIS 


the  left  axilla;  occasionally  an  attenuated  diastolic  bruit  is  audible 
over  the  subclavian  and  the  carotid  arteries.  The  murmur  begins 
with  diastole,  and  its  greatest  intensity  coincides  with  the  second 
sound,  after  which  it  is  prolonged,  as  a  gradual  diminuendo, 
generally  throughout  the  entire  diastolic  period,  but  occasionally 
subsiding  before  its  completion.  The  quality  of  the  sound  is  more 
often  soft  and  blowing  than  loud  and  rasping,  and  its  pitch  is 
tolerably  high ;  rarely,  it  is  distinguished  by  an  unmistakably  musical 
tone,  in  which  event  considerable  valve  laceration  is  suggested.  The 
murmur  may  be  so  faint  as  to  be  almost  inaudible — indeed,  extensive 
leakage  at  the  aortic  orifice  sometimes  exists  with  no  murmur  at 
all — and  its  intensity  is  no  criterion  of  the  extent  of  the  endocardial 
damage. 
The  aortic  second  sound  is  partly  or  wholly  replaced  by  the  murmur, 


Fig.  177. — Mechanism  of  the  Flint  murmur  of  aortic  regurgitation. 

persistence  of  the  second  sound  probably  meaning  a  less  serious 
aortic  leakage  than  total  masking  of  the  tone  by  the  murmur. 
In  judging  the  intensity  of  the  aortic  second  sound  one  should  always 
auscultate  over  the  carotid  artery,  in  order  to  eliminate  the  pulmonic 
second  sound,  inaudible  in  this  situation.  The  first  sound  at  the 
base  may  be  distinct  and  clear  and  loud,  but  more  often  it  is  obscured 
by  a  systolic  bruit  attributable  to  several  causes — roughening  of  the 
aortic  leaflets,  atheroma  or  dilatation  of  the  aorta,  true  stenosis  of  the 
aortic  orifice,  or  anemia.  The  addition  of  this  systolic  sound  pro- 
duces the  familiar  "see-saw"  or  "to-and-fro"  murmur  of  a  double 
aortic  lesion.  At  the  apex  the  first  sound  is  likely  to  be  muffled, 
or  perhaps  overshadowed  by  the  bruit  of  mitral  leakage,  either 
relative  or  organic.  The  apical  second  sound  is  unduly  feeble,  and 
not  uncommonly  tinctured  with  the  diastolic  bruit  reflected  thence 
from  the  base.  The  rough  presystolic  murmur  of  Flint  (see  p.  382) 
is  also  audible  at  the  apex  in  a  certain  proportion  of  cases — in 
about  50  per  cent.,  says  Thayer  (Fig.  177).  In  certain  instances 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM  457 

auscultation  over  the  femoral  artery  reveals  a  sudden  systolic  thud 
coincident  with  the  abrupt  distention  of  the  arterial  wall  by  the 
impact  of  the  blood-column,  which  sound,  appreciable  only  when 
very  gentle  stethoscopic  pressure  is  used,  gives  way  to  a  physiologic 
constriction  murmur  when  the  pressure  is  increased.  Duroziez's 
sign,  consisting  of  this  normal  systolic  bruit  plus  a  diastolic  murmur 
of  arterial  reflux,  can  often  be  developed  by  carefully  graduating 
the  pressure  over  the  vessel  until  it  is  constricted  to  the  exact  degree 
essential  for  the  creation  of  this  distinctive  double  sound.  (See 
p.  393.)  Exceptionally,  auscultation  over  the  femorals  reveals  a 
faint  double  sound,  not  unlike  that  of  the  heart-beat — Traube's  sign. 

Diagnosis. — Arterial  throbbing,  a  tumultuous  apex-beat,  col- 
/apsing  radial  and  visible  capillary  pulses,  enlargement  of  the  left 
ventricle,  and  a  diastolic  aortic  murmur,  propagated  downward  and 
toward  the  left,  unmistakably  indicate  Corrigan's  disease,  apart  from 
the  less  constant  corroborative  signs  of  this  lesion  that  also  may 
be  demonstrable.  Subjects  ot  aortic  incompetence  usually  suffer 
from  throbbing  headache,  vertigo,  phosphenes,  and  tinnitus,  while 
precordial  pain,  even  true  angina,  is  more  common  in  this  lesion 
than  in  any  other  type  of  valvular  affection.  Aortic  disease,  espec- 
ially regurgitation,  is  not  infrequently  attended  by  most  distressing 
mental  symptoms — insomnia,  dreadful  dreams,  melancholia,  suicidal 
mania,  and  delirium.  In  this  connection  it  may  be  noted  that  so- 
called  "  heart-disease  delirium  "  may  be  counterfeited  by  the  mental 
symptoms  due  to  the  toxic  effect  of  digitalis,  as  H.  O.  Hall  has 
pointed  out. 

The  differentiation  of  aortic  regurgitation  from  pulmonary  regurgi- 
tation hinges  upon  the  arterial  phenomena  and  the  nature  of  the 
cardiac  structural  changes,  the  details  of  which  are  dealt  with  in 
another  place.  (See  p.  473.)  In  a  preceding  section  (see  pp.  378 
and  391)  the  characteristics  of  diastolic  anemic  and  cardiorespiratory 
murmurs  sometimes' audible  at  the  base  of  the  heart  are  considered. 

The  Flint  murmur  and  the  mitral  stenotic  bruit  have  been  com- 
pared in  the  diagnosis  of  mitral  stenosis.  (See  p.  448.) 

AORTIC  STENOSIS 

Clinical  Pathology. — Stenosis,  like  insufficiency  of  the  aortic 
orifice,  is  more  frequently  attributable  to  a  slow  sclerosis  than  to 
frank  endocardial  inflammation,  and  is  prone  to  affect  men  past 
the  prime  of  life,  in  whom  more  or  less  general  arterial  fibrosis 
exists.  In  rare  instances  the  obstructive  lesion  is  the  relic  of  an 
antenatal  process.  Pure  aortic  stenosis  is  the  rarest  acquired 


458 


PHYSICAL   DIAGNOSIS 


valvular  defect  of  the  left  heart,  for  in  the  vast  majority  of  stenoses 
there  is  also  reflux  of  blood  through  the  orifice. 


Wall  of  aorta 
Stenotic  orifice  of  aorta 


>.    JL  Atheromatous  wall  of 
aorta 


Vegetations  of  surface 
of  valve  cusp 


Fig.  178. — Aortic  stenosis  (Jefferson  Hospital  Laboratories). 

Obstruction  to  the  flow  of  blood  from  the  left  ventricle  into  the 
aorta  ordinarily  is  due  to  rigidity  and  thickening  of  the  semilunai 


Systole 
Fig.   179. — Mechanism  of  the  murmur  of  aortic  stenosis. 

cusps,  whereby  they  fail  closely  to  hug  the  aortic  wall  during  sys- 
tole, and  hence  impede  the  outflowing  blood-stream  propelled  by 
the  ventricular  contractions  (Fig.  1 79).  In  some  cases  the  orifice  is 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM 


459 


obstructed  by  vegetative  excrescences,  by  simple  adhesion  of  the 
valve  borders,  or  by  the  formation,  by  fusion  of  the  cusps,  of  a 
constricted  funnel-like  communication  between  the  ventricle  and  the 
aorta.  Calcification  of  the  valve-leaflets,  as  well  as  vegetative  and 
calcareous  changes  in  the  interventricular  septum  at  the  attachment 
of  the  aortic  mitral  cusp,  may  also  develop.  A  type  of  aortic  stenosis, 


Fig.  180.— Dilatation  of  the  aortic  arch  (Jefferson  Hospital). 

due  not  to  valvular  deformity,  but  simply  to  fibrocalcareous  con- 
striction of  the  aortic  ring,  also  has  been  described.  In  congenital 
lesions  it  is  the  rule  to  find  adhesion  and  thinning  of  the  aortic  cusps 
with  little  or  no  evidence  of  atheroma ;  or  the  defect  may  be  a  so- 
called  subaortic  stenosis,  consisting  of  a  constriction  of  the  ventric- 
ular chamber  by  a  ring  of  endocardial  thickening  situated  below 
the  aortic  cusps — a  process  comparable  to  the  conal  type  of  pul- 
monary stenosis  (q.  v.  i.).  Occasionally,  neither  valve  nor  ring  is 


460  PHYSICAL   DIAGNOSIS 

affected,  but  the  aorta  immediately  beyond  the  latter  is  dilated — a 
condition  known  as  relative  aortic  stenosis,  though  obviously  "di- 
latation of  the  aorta"  is  the  better  term  for  the  condition.  The 
walls  of  the  aortic  arch  are  very  commonly  the  seat  of  fibrocalca- 
reous  degeneration. 

The  immediate  effect  of  aortic  obstruction  is  a  gradual  and 
progressive  thickening  of  the  wall  of  the  left  ventricle,  primarily 
unattended  by  dilatation.  This  change,  one  of  so-called  simple 
hypertrophy,  is  referable  to  the  increased  work  thrown  upon  the 
ventricle  in  its  endeavor  to  force  the  blood  through  an  unduly  narrow 
aortic  opening.  Later,  however,  the  ventricle  tends  to  give  way 
under  the  incessant  strain  and  to  suffer  myocardial  degeneration, 
due  to  coronary  artery  occlusion,  and  in  consequence  it  dilates, 
perhaps  so  decidedly  that  relative  mitral  leakage  ensues,  and  in 
time  the  left  auricle,  .the  pulmonary  circuit,  and  the  right  ventricle 
are  affected  by  the  back  pressure. 

Physical  Signs. — Inspection. — The  subject  of  aortic  stenosis 
shows  little  or  no  evidence  of  a  diseased  heart  so  long  as  the  left 
ventricle  does  not  flag  and  the  mitral  valve  remains  tight,  but  when 
these  structures  give  way  signs  of  an  embarrassed  pulmonary  circula- 
tion, already  described,  appear.  Anemic  pallor  is  likely  to  develop 
in  the  course  of  time,  and  in  arteriosclerotic  patients  exaggerated 
prominence  and  tortuosity  of  the  hardened  surface  vessels  attract 
attention  at  first  glance.  The  apical  impulse,  apparently  of  fair 
force,  is  dislocated  obliquely  downward  and  somewhat  outward;  or, 
as  in  old  emphysematous  individuals,  the  apex-beat  may  be  looked 
for  in  vain. 

Palpation. — With  tolerable  constancy  a  rather  coarse  systolic 
thrill,  usually  most  intense  at  the  aortic  cartilage,  is  felt  at  the  cardiac 
base,  and,  rarely,  over  the  larger  arteries  near  the  surface.  The 
apex-beat,  if  palpable,  is  regular,  slow,  deliberate,  and  heaving  until 
the  disturbing  effects  of  left  ventricular  failure  come  into  play. 

The  pulse  of  pure  aortic  stenosis  (pulsus  tardus)  has  a  slow  rate, 
moderate  or  small  volume,  normal  rhythm,  and  prolonged,  deliberate 
rise  and  fall.  The  tracing  of  such  a  pulse  is  quite  distinctive,  the 
wave  being  of  diminished  height,  and  composed  of  an  unduly  ob- 
lique ascent,  a  blunt  apex,  and  a  gradually  falling  down-stroke,  with 
indistinct  secondary  oscillations.  Or,  the  tracing  may  register  the 
double  apex  of  a  pulsus  bisferiens,  suggestive  of  a  double-phased 
contraction  of  the  ventricle;  while  sometimes  the  notched  upstroke 
of  anacrotism  is  shown.  (See  Fig.  130,  ix,  x,  xiv;  p.  341.) 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  461 

Percussion. — The  downward  and  outward  extension  of  cardiac 
dulness  is  proportionate  to  the  degree  of  left  ventricular  enlargement, 
but  in  the  average  case  of  aortic  stenosis  the  precordial  limits  are 
much  more  restricted  than  in  Corrigan's  disease.  Impairment  of 
pulmonary  resonance  at  the  right  of  the  sternum  may  be  detected 
as  a  late  finding  should  secondary  hypertrophy  of  the  right  ventricle 
occur. 

Auscultation. — Aortic  stenosis  is  attended  by  a  systolic  basic 
murmur  having  its  punctum  maximum  at  the  aortic  cartilage,  whence 
it  is  transmitted  into  the  carotid  arteries,  and  in  some  instances  over 
the  entire  precordia;  most  exceptionally,  it  is  also  audible  alongside 
the  spine,  over  the  course  of  the  descending  thoracic  aorta.  Typically, 
the  bruit  is  loud  and  rough  and  rasping;  atypically,  it  is  soft  and  blow- 
ing, or  musical.  The  aortic  first  sound  is  likely  to  be  masked  by  the 
murmur,  particularly  when  this  synchronous  tone  is  notably  harsh 
and  intense.  The  aortic  second  sound  is  more  or  less  muffled  and 
enfeebled,  sometimes  to  the  point  of  actual  extinction,  this  highly 
suggestive  sign  of  aortic  obstruction  depending  upon  rigidity  and 
thickening  of  the  valve-leaflets.  As  a  rule,  the  aortic  second  sound 
is  still  further  obscured  by  a  diastolic  bruit,  owing  to  the  frequency 
of  an  associated  leakage  at  the  aortic  orifice.  The  first  sound  at  the 
apex  is  dully  muscular  in  quality,  and  the  second  sound  in  this 
situation  is  indistinct,  or  perhaps  blended  with  the  transmitted 
bruit  of  a  coexisting  reflux. 

Diagnosis. — A  systolic  basic  thrill,  an  aortic  systolic  murmur 
propagated  into  the  neck,  and  impairment  of  the  aortic  second 
sound  together  determine  the  diagnosis  of  aortic  stenosis,  of  which 
lesion  moderate  enlargement  of  the  left  ventricle  and  a  pulse  indicating 
slow,  deliberate,  and  often  double-phased  ventricular  systoles  are 
highly  corroborative.  True  aortic  stenosis  is  unusual  as  an  isolated 
defect,  whereas  aortic  systolic  murmurs,  most  often  symptomatic 
of  atheroma  or  dilatation  of  the  aortic  arch,  or  of  some  functional 
inadequacy  of  the  heart,  are  very  common. 

Atheroma  of  the  aorta  may  precisely  simulate  aortic  stenosis  in  so 
far  as  the  time,  quality,  and  transmission  of  the  bruit  are  concerned, 
but  in  atheroma  a  thrill  is  exceptional,  suggestive  pulse  changes  are 
lacking,  arteriosclerotic  hypertrophy  of  the  left  ventricle  exists,  and, 
most  important  of  all,  the  aortic  second  sound  rings  clearly  at  the 
base  of  the  heart.  Well-defined  arteriosclerosis  is  in  favor  of  aortic 
atheroma,  though  the  arteries  are  hard  in  many  examples  of  stenosis. 

Dilatation  of  the  aortic  arch,  whether  diffuse  or  aneurismal,  also 
accounts  for  an  aortic  systolic  murmur  which  is  conducted  into  the 


462  PHYSICAL    DIAGNOSIS 

neck,  as  well  as  for  a  corresponding  thrill,  in  many  instances. 
In  simple  dilatation  of  the  aorta  one  looks  for  systolic  pul- 
sation and  unnatural  dulness  over  the  ascending  aortic  arch, 
throbbing  in  the  suprasternal  notch,  a  pulse  of  fairly  good  volume, 
and  either  accentuation  of  the  aortic  second  sound  or  its  modification 
by  a  bruit  of  concomitant  aortic  leakage.  In  differentiating  aneurism 
of  the  aorta,  attention  should  be  directed  to  certain  distinctive  signs 
of  this  affection:  an  area  of  circumscribed  dulness  affording  systolic 
pulsation  and  diastolic  shock,  a  loud,  low-pitched  aortic  second 
sound,  and  pressure  symptoms  affecting  the  pulses,  the  pupils,  and 
the  voice.  The  value  of  these  findings  as  diagnostic  criteria  is  dealt 
with  more  fully  in  another  place.  (See  p.  489.)  The  discrimina- 
tion between  aortic  stenosis  and  mitral  regurgitation,  pulmonary 
stenosis,  and  patent  ductus  arteriosus  is  given  under  these  headings. 
(See  pp.  439,  470,  and  475.) 

TRICUSPID  REGURGITATION 

Clinical  Pathology. — Tricuspid  regurgitation,  due  to  organic 
valvular  lesions  or  to  relative  muscular  deficiency,  is  established  when, 
during  systole  of  the  right  ventricle,  blood  escapes  thence  through 
an  incompetent  tricuspid  orifice  into  the  right  auricle,  as  well  as 
forward  into  the  normal  outlet  through  the  pulmonary  artery. 
Organic  tricuspid  regurgitation  is  comparatively  uncommon  as  a 
clinical  finding,  though  it  is  not  improbable,  as  Bramwell  suggests, 
that  the  tricuspid  leaflets  are  frequently  invaded  by  inflammatory 
processes  which  abate  without  permanently  crippling  the  valve 
mechanism,  owing  to  the  tendency  of  such  lesions  to  undergo  perfect 
resolution  under  the  low  pressure  of  the  lesser  blood  circuit.  The 
organic  defects  accountable  for  tricuspid  leakage  do  not  differ  mater- 
ially, either  in  origin  or  in  kind,  from  those  productive  of  mitral 
regurgitation,  endocarditis  and  sclerotic  degeneration  of  the  cusps 
and  their  tendinomuscular  attachments  being  the  factors  inter- 
fering with  the  integrity  of  the  valve.  Fibrous  induration,  thick- 
ening, and  puckering  of  the  valve  segments,  shortening  of  the  chordae 
tendineae,  and  sclerosis  of  the  musculi  papillares  are  familiar  patho- 
logic findings;  or  the  free  auricular  border  of  the  valve  may  be  the 
seat  of  vegetations  indicating  endocardial  inflammation  of  the  acute 
or  chronic  benign  variety,  or  of  the  malignant  type;  in  the  latter  the 
mural  endocardium  is  also  most  likely  to  be  similarly  implicated. 
Sclerotic  degeneration  is  commoner  at  the  tricuspid  orifice  than 
active  inflammation, — just  the  reverse  of  the  conditions  prevailing  at 
the  mitral  opening, — such  changes  supervening  as  the  result  of  per- 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  463 

sistent  pulmonary  hypertension,  and  consequently  being  secondary 
to  mitral  lesions  (especially  stenotic),  left  ventricular  dilatation, 
arterial  sclerosis,  and  chronic  indurative  affections  of  the  lungs,  all 
of  which  obstruct  the  pulmonary  current,  and  by  so  doing  excite 
habitually  high  tension  within  the  right  ventricle.  Traumatic 
tricuspid  leakage,  due  either  to  cusp  laceration  or  to  tendinous  rupture, 
is  most  unusual,  owing  to  the  natural  tendency  of  the  right  auriculo- 
ventricular  sphincter  to  stretch  and  thus  permit  a  "safety-valve" 
regurgitation,  under  sudden  and  acute  intraventricular  stress  (v.  i.). 

Relative  tricuspid  regurgitation,  consequent  to  muscular  inadequacy, 
is  an  exceedingly  common  lesion,  consisting  essentially  of  right 
ventricular  dilatation,  stretching  of  the  tricuspid  ring,  and  relative 
shortening  of  the  chordae  tendineae  and  musculi  papillares,  as  the 
result  of  which  the  valve  cusps  cannot  approximate  accurately  with 
systole,  and  hence  permit  reflux  into  the  right  auricle  at  this  time. 
So-called  "safety-valve  regurgitation, "  a  truly  conservative  condition, 
occurs  at  the  tricuspid  orifice  when,  as  the  result  of  increased  pul- 
monary tension  and  distention  of  the  right  ventricle,  the  tricuspid 
sphincter  enlarges  so  as  to  permit  a  backward  leakage  which  relieves 
the  stress  upon  the  ventricular  wall  and  lowers  the  tension  of  the 
pulmonary  circulation.  This  natural  tendency  of  the  tricuspid  valve 
automatically  to  ease  the  strain  upon  the  right  heart  is  well  illustrated 
by  the  transient  tricuspid  leakage  provoked  by  violent  muscular 
exercise.  Relative  tricuspid  regurgitation  may  attend  true  organic 
valvular  disease,  but  it  sometimes  exists  with  perfectly  healthy  valves; 
its  persistence  is  determined  by  the  character  of  the  underlying  cause. 
Relative  incompetence  of  the  tricuspid  valve  from  muscular  deficiency 
of  the  right  ventricle  is  a  common  secondary  development  in  fever, 
anemia,  toxemia,  and  other  factors  of  myocardial  relaxation,  mal- 
nutrition, and  degeneration;  it  accompanies  conditions  of  heightened 
pulmonary  tension  consecutive  to  pulmonary  fibrosis  and  emphysema, 
mitral  disease,  and  left  ventricular  dilatation,  and  develops  in  con- 
sequence of  pulmonary  stenosis. 

Physical  Signs. — Inspection. — Free  tricuspid  leakage  attended 
by  right  auricular  dilatation  cannot  long  exist  without  producing 
unmistakable  evidences  of  an  impeded  venous  circulation,  such  as 
cyanosis,  edema,  and  distention  and  pulsation  of  the  visible  veins. 
Dyspnea  and  cough  are  also  common  features,  either  as  forerunners 
of  the  right-sided  heart  failure,  or  arising  indirectly  from  this  accident, 
by  the  extension  of  the  back  pressure  to  the  lungs  through  the  sys- 
temic capillaries  and  arteries.  The  patient's  cyanosis  varies  with 
the  inadequacy  of  blood  aeration  existing  in  the  individual  case; 


464  PHYSICAL    DIAGNOSIS 

the  edema,  commonly  beginning  as  dropsy  of  the  feet  and  ankles, 
ultimately  tends  to  implicate  the  serous  sacs  in  the  guise  of  ascites 
and  hydrothorax,  the  latter  being  prone  to  affect  the  right  pleural 
cavity.  Turgescence  of  the  small  veins  of  the  surface,  in  some 
instances  most  conspicuous,  is  detected  by  inspection  of  the  upper 
anterior  thoracic  wall  and  the  extremities.  The  external  jugular 
veins  are  unnaturally  distended,  and,  when  emptied  by  pressure, 
fill  from  below;  they  may  show  the  systolic  pulsation  of  a  positive 
venous  pulse,  the  presystolic  pulsation  of  a  negative  venous  pulse, 
or  a  double  jugular  pulsation  due  to  the  coexistence  of  both  types 
of  pulse.  (See  Venous  Pulse,  p.  346.) 

Palpation. — There  is  epigastric  pulsation,  due  to  enlargement  of 
the  right  ventricle,  and  varying  in  force  with  the  strength  of  this 
chamber's  contractions.  Palpation  of  the  liver  discovers  a  positive 
venous  pulse  over  this  organ  if  the  reflux  venous  waves  created  by 
the  ventricular  systoles  are  conducted  thereto.  The  distinctive 
expansile  property  of  this  type  of  pulsation  is  to  be  distinguished 
from  the  mere  lifting  impulse  of  a  liver  jogged  by  the  impact  of  a 
hypertrophied  right  ventricle;  bimanual  palpation,  raising  the  liver 
with  one  hand  and  feeling  its  anterior  surface  with  the  other,  is  the 
most  certain  method  of  appreciating  these  differences. 

The  pulse  of  tricuspid  regurgitation  is  in  no  wise  characteristic, 
such  irregularities  as  may  exist  being  attributable  to  concomitant 
lesions  of  the  left  heart.  A  relatively  feeble  radial  pulse  on  the  right 
side  suggests  compression  of  the  right  subclavian  artery  by  an 
enlarged  right  auricle  (Popoff). 

Percussion. — Owing  to  enlargement  of  the  right  heart,  cardiac 
dulness  extends  unnaturally  beyond  the  right  border  of  the  sternum 
and  downward,  while  more  often  than  not  one  also  finds  impairment 
of  resonance  due  to  enlargement  of  the  left  ventricle.  Congestion 
of  the  liver  produces  lengthening  of  the  vertical  lines  of  hepatic 
flatness,  the  edge  of  the  organ  often  reaching  far  below  the  costal 
margin. 

Auscultation. — The  murmur  of  tricuspid  incompetence  is  most 
distinct  over  the  lower  part  of  the  sternum,  as  a  soft,  blowing,  systolic 
sound,  which,  though  not  propagated  along  hard-and-fast  lines,  is 
audible  over  a  roughly  triangular  region  lying  between  the  tricuspid 
area,  the  right  midaxillary  line,  and  the  manubrium  (Fig.  158); 
inconstantly  the  bruit,  enfeebled,  is  also  heard  in  the  neighborhood 
of  the  apex.  The  punctum  maximum  of  the  murmur  is  commonly 
situated  at  the  conventional  tricuspid  area,  but  as  the  right  ventricle 
undergoes  changes  in  size  and  shape,  the  point  correspondingly 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM  465 

shifts — to  the  xiphoid  cartilage,  to  the  left  sternal  edge  over  the  fifth 
or  sixth  costal  cartilages,  or  to  the  right  sternal  edge  over  the  third, 
fourth,  or  fifth  cartilages.  The  tricuspid  first  sound  is  masked  by 
the  attendant  murmur,  but  only  exceptionally  is  it  entirely  suppressed. 
In  pure  tricuspid  leakage  the  pulmonic  second  sound  is  enfeebled; 
accentuation  and  reduplication  suggest  coexistent  left-sided  disease. 
Auscultation  over  a  pulsating  cervical  vein  may  reveal  a  systolic  venous 
bruit.  It  is  the  rule  to  find  at  the  apex  signs  of  coexisting  mitral 
disease  to  which  the  right-sided  leakage  is  secondary. 

Diagnosis. — A  systolic  (ventricular)  jugular  and  hepatic  pulse, 
a  tricuspid  systolic  murmur  conducted  toward  the  right,  enfeeblement 
of  the  pulmonic  second  sound,  enlargement  of  the  right  heart,  and 
evidences  of  venous  obstruction  are  the  typical  findings  of  this  lesion. 
Moderate  tricuspid  leakage,  so  long  as  the  tone  of  the  right  auricle 
is  adequate,  affords  none  of  the  foregoing  venous  phenomena,  and 
in  such  an  instance  there  may  be  merely  a  soft  systolic  whiff,  audible 
over  the  lower  part  of  the  sternum.  Furthermore,  it  is  probably 
true  that  tricuspid  regurgitation,  especially  of  the  muscular  or  "safety- 
valve"  types,  not  infrequently  gives  rise  to  no  physical  signs  whatever. 

TRICUSPID  STENOSIS 

Clinical  Pathology. — This  exceedingly  rare  lesion  may  be  of 
acquired  or  of  congenital  origin,  and  in  either  event  is  almost  invaria- 
bly associated  with  other  cardiac  damage,  examples  of  pure  isolated 
tricuspid  stenosis  being  most  unusual.  The  acquired  form,  making 
up  the  great  majority  of  all  cases,  occurs  most  commonly  during  the 
second  decade  of  life  in  women  who  give  a  history  of  rheumatic 
endocarditis,  and  who  also  suffer  from  mitral  stenosis.  The  mi- 
tral affection,  inducing  protracted  hypertension  within  the  right 
ventricle,  and  hence  irritation  of  the  tricuspid  segments,  is  the 
primary  cause  of  many  tricuspid  stenoses,  though  there  is  good 
reason  for  believing  that  sometimes  both  auriculoventricular  valves 
are  simultaneously  attacked  by  a  wide-spread  inflammation.  Aside 
from  stenosis  due  to  well-defined  inflammation  of  the  endocardium, 
the  defect  occasionally  arises  in  consequence  of  slow  valvular  sclerosis. 
In  general,  the  structural  changes  affecting  the  tricuspid  valve 
mechanism  are  similar  to  those  of  its  mitral  counterpart,  except  that 
on  the  right  side  of  the  heart  the  degree  of  constriction  is  likely  to  be 
less  advanced,  probably  because  the  mitral  lesion  is  usually  primary 
and,  therefore,  older  than  the  tricuspid  defect,  and,  unlike  the  latter, 
tends  to  persist  and  to  progress,  rather  than  to  undergo  resolution. 
30 


466  PHYSICAL   DIAGNOSIS 

Congenital  tricuspid  stenosis,  the  product  of  fetal  endocarditis  or  of 
developmental  anomaly,  is  less  common  than  the  acquired  type. 
It  is  almost  invariably  attended  by  other  defects  of  cardiac  develop- 
ment— perforation  of  the  ventricular  septum,  patency  of  the  foramen 
ovale  or  the  ductus  arteriosus,  and  stenoses  of  other  orifices. 

Owing  to  the  increased  force  the  right  auricle  must  exert  in  pro- 
pelling its  contents  through  the  stenotic  tricuspid  orifice,  the  walls 
of  this  chamber  hypertrophy  and  later  dilate,  for  the  myocar- 
dium weakens  under  the  incessant  stress,  so  that  the  auricle  be- 
comes habitually  overfilled  by  residual  blood,  and,  in  most  instances, 
overdistended  by  a  systolic  reflux  stream  from  the  right  ventricle,  due 
to  concurrent  tricuspid  incompetence.  Most  extraordinary  enlarge- 
ment of  the  auricle  and  thinning  of  its  walls  are  sometimes  observed 
as  the  result  of  these  several  factors.  The  venous  obstruction 
depending  upon  auricular  failure  has  already  been  described.  (See 
p.  432.)  The  effect  of  pure  tricuspid  stenosis  is  to  diminish  the  size 
of  the  right  ventricle,  but,  as  a  matter  of  fact,  this  chamber  is  nearly 
always  found  to  be  hypertrophied  and  dilated,  in  consequence  of  an 
attendant  mitral  lesion,  which  also  accounts  for  the  pulmonary  con- 
gestion, when  this  exists.  Arterial  anemia  develops  should  the 
right  ventricular  output  of  blood  be  inadequate  for  the  needs  of  the 
pulmonary  circulation,  the  left  side  of  the  heart,  and  the  greater 
blood  circuit. 

Physical  Signs.1 — Inspection. — Chronic  cyanosis,  well-defined 
turgescence  of  the  surface  veins,  and  persistent  dropsy  are  most 
constant,  yet  not  pathognomonic,  signs  of  tricuspid  obstruction. 
Assuming  that  the  tricuspid  orifice  does  not  leak,  there  is  jugular 
distention,  unattended  by  systolic  (positive)  pulsation,  though  a 
presystolic  (negative)  flicker  is  sometimes  visible  should  the  force 
of  the  right  auricle  be  sufficient  to  propel  a  backward  venous  wave. 

Palpation. — Occasionally  a  short,  purring,  presystolic  thrill,  end- 
ing in  a  sharp,  systolic  impulse,  is  appreciable  over  the  xiphoid  ap- 
pendix, but  there  is  no  epigastric  throbbing  so  long  as  the  right 
ventricle  does  not  hypertrophy.  The  edge  of  the  liver  is  palpable 
and,  rarely,  pulsatile  below  the  right  costal  arch,  and  the  skilful 
use  of  the  kymograph  may  show  a  presystolic  hepatic  pulse  wave, 
if  the  right  auricle  be  hypertrophied  (Mackenzie).  The  pulse  in 

1  For  the  purpose  of  description,  it  is  thought  best  to  give  the  signs  of  a  pure 
tricuspid  stenosis.  The  reader  should  appreciate,  however,  that  in  actual 
practice  this  rare  lesion,  if  met  with  at  all,  is  nearly  always  attended  by  other 
valvular  defects — by  mitral  stenosis  in  fully  90  per  cent,  of  cases.  Isolated 
tricuspid  stenosis  made  up  but  about  7  per  cent,  of  Herrick's  154  collected 
records  of  this  affection. 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  467 

the  radials  may  exhibit  no  deviation  from  normal,  or  the  beats 
may  be  accelerated,  arhythmic,  small,  and  forceless. 

Percussion. — Right  auricular  enlargement  accounts  for  consider- 
able extension  of  cardiac  dulness  at  the  base,  particularly  upward 
and  to  the  right  of  the  sternum.  Hepatic  dulness  is  increased 
commensurately  with  the  existing  degree  of  hepatic  engorgement. 

Auscultation. — A  short,  rough  presystolic  murmur,  ending  in  a 
sharp  first  sound  and  restricted  to  the  tricuspid  area,  is  heard  in 
obstruction  of  the  tricuspid  orifice.  The  punctum  maximum  of  this 
murmur,  which  is  not  propagated  thence,  corresponds  variously 
to  the  base  of  the  ensiform  or  to  either  edge  of  the  sternum,  and,  as 
in  its  mitral  equivalent,  the  sound  may  be  either  strictly  presystolic 
in  time,  or  it  may  begin  directly  after  the  second  sound,  running 
through  the  entire  diastolic  period  with  a  distinct  crescendo  just 
before  the  first  sound.  The  cardiac  tones  at  the  base  are  enfeebled, 
should  there  be  anemia  of  the  pulmonary  circuit,  and,  consequently, 
reduction  in  the  volume  of  blood  within  the  left  heart. 

Diagnosis. — A  presystolic  murmur  and  a  sharp  first  sound  in  the 
tricuspid  area,  with  enlargement  of  the  right  side  of  the  heart,  mean 
stenosis  of  the  tricuspid  orifice,  provided  that  it  is  possible  to  exclude 
concomitant  mitral  obstruction  (q.  v.).  The  frequent  coexistence 
of  the  latter  lesion,  which  masks  the  tricuspid  signs,  largely  accounts 
for  the  common  failure  to  recognise  tricuspid  stenosis  during  life. 
Corroborative  evidence  of  tricuspid  stenosis  consists  of  cyanosis, 
edema,  hepatic  enlargement,  turgid  pulsating  jugulars,  and  a  presys- 
tolic thrill  over  the  ensiform.  According  to  the  elder  Broadbent, 
in  the  face  of  signs  indicating  pure  mitral  stenosis,  the  presence  of 
extensive  and  persistent  dropsy  is  sufficient  grounds  for  believing  that 
the  tricuspid  orifice  is  likewise  obstructed. 

PULMONARY  STENOSIS 

Clinical  Pathology. — This  very  rare  defect  is  almost  invariably 
of  congenital  origin,  being  the  most  frequent  form  of  valvular  disease 
attributable  to  developmental  imperfection  or  to  fetal  endocarditis. 
Ordinarily,  the  narrowing  is  due  to  adhesion  of  the  cusps  and  con- 
traction of  the  muscular  sphincter,  with  more  or  less  induration, 
thickening,  and  rigidity  of  the  leaflets;  but  vegetative  excrescences, 
in  the  exceptional  case,  may  be  virtually  the  sole  cause  of  the  obstruc- 
tion. Or  the  stenosis  may  implicate  the  conus  arteriosus,  whose 
walls  are  thickened  and  indurated  by  a  fibroid  myocarditis  excited 
by  the  extension  of  a  primary  endocardial  inflammation.  Rarely, 
endarteritic  obstruction  of  the  pulmonary  artery  is  the  initial  seat  of 


468  PHYSICAL   DIAGNOSIS 

the  stenosis,  and  in  some  instances  a  fault  of  development  results 
in  the  virtual  occlusion  of  the  first  part  of  this  vessel  and  also 
of  the  pulmonic  orifice.  In  congenital  cases  the  valvular  defect  is 
generally  associated  with  other  antenatal  malformations,  such  as 
patency  of  the  ductus  arteriosus  or  the  foramen  ovale,  and  perforation 
of  the  interventricular  septum;  frequently  the  tricuspid  orifice  is 
likewise  obstructed;  and,  from  their  very  nature,  many  of  the  lesions 
causing  pulmonary  stenosis  also  cause  incompetence  of  this  valve. 
In  the  few  recorded  examples  of  acquired  pulmonary  stenosis  benign 
and  malignant  endocarditis,  gumma,  and  injury  to  the  precordia 
have  figured  as  the  exciting  causes.  In  endocarditic  stenoses  the 
acute  specific  infections,  and  especially  the  eruptive  fevers,  appear 
to  be  more  active  factors  than  rheumatism;  this  is  equally  true  of 
regurgitant  lesions  at  the  pulmonic  orifice,  and  in  its  relative  insus- 
ceptibility to  rheumatic  valvulitis  the  pulmonic  valve  differs  from  the 
valves  of  the  other  cardiac  orifices.  In  a  pure  pulmonary  stenosis 
of  moderate  degree  hypertrophy  of  the  right  ventricle  is  the  primary, 
if  not  the  only,  structural  change  induced,  but  if  the  obstruction  be 
extreme,  or  if  it  be  combined  with  regurgitation,  ventricular  dilatation 
and  relative  tricuspid  leakage  soon  supervene.  This,  of  course, 
leads  to  embarrassment  of  the  venous  flow  to  the  right  auricle,  the 
evidences  of  which  have  been  sufficiently  considered  in  a  preceding 
paragraph.  Pulmonary  stenosis,  whether  congenital  or  acquired, 
is  regarded  as  a  predisposing  cause  of  tuberculosis  of  the  lungs, 
whose  blood-supply  and  nutrition  are  interfered  with  by  the  obstruc- 
tion to  the  blood  flow  from  the  right  ventricle. 

Dilatation  of  the  pulmonary  artery,  the  orifice  remaining  of  normal 
size,  establishes  a  condition  of  relative  pulmonary  stenosis, 

Physical  Signs. — Inspection. — Striking  cyanosis,  urgent  dyspnea, 
and  extensive  venous  turgescence  commonly  attend  pulmonary 
stenosis  of  the  congenital  type,  but  in  acquired  cases  with  adequate 
compensation  the  breathing  is  not  greatly  embarrassed,  anemic 
pallor  is  more  conspicuous  than  cyanosis,  and  the  other  consequences 
of  venous  obstruction  are  not  likely  to  become  prominent.  The 
epigastrium  heaves  systolically  with  undue  force,  owing  to  the  impact 
of  the  hypertrophied  right  ventricle,  and>?most  writers  speak  of  pre- 
cordial  bulging  from  the  same  cause. 

Palpation. — The  hand  applied  to  the  base  of  the  heart  appreciates 
a  systolic  thrill  of  variable  quality  and  of  maximum  intensity  in  the 
pulmonic  area,  while  palpation  over  the  subcostal  angle  shows  that 
the  right  ventricle  is  contracting  with  excessive  force. 

The  pulse  in  the  radials,  though  prone  to  become  accelerated, 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  469 

small,  and  arhythmic,  gives  no  specific  indication  of  the  valvular 
lesion  under  consideration. 

Percussion. — An  extension  of  cardiac  dulness,  relating  primarily 
to  right  ventricular  hypertrophy  and  later  to  right  auricular  dilatation, 
is  an  important  corroborative  sign  of  pulmonary  stenosis.  The 
hepatic  area  does  not  increase  in  size  until  the  supervention  of  venous 
engorgement  of  the  liver. 

Auscultation. — Pulmonary  stenosis  creates  a  systolic  murmur 
having  its  point  of  maximum  intensity  in  the  second  and  third  inter- 
spaces at  the  left  sternal  border,  and  propagated  thence  upward 
toward  the  left  clavicle,  but  not  into  the  arterial  trunks  of  the  neck 
(Fig.  159).  If  the  bruit  be  intense,  its  area  of  audibility  may  extend 
over  a  considerable  part  of  the  anterior  chest- wall,  but  invariably  it  is 
more  distinct  on  the  left  than  on  the  right  side,  being  conducted  along 
the  pulmonary  artery  and  its  branches  rather  than  by  the  aorta.  The 
murmur  of  pulmonary  obstruction  ordinarily  is  intense,  rough,  and 
superficial,  effectually  masking  the  pulmonic  first  sound,  though 
exceptionally  it  is  a  feeble,  soft,  and  distant  tone.  The  pulmonic 
second  sound  is  either  muffled  and  impure,  or  entirely  suppressed, 
but  the  sounds  in  the  aortic  area  are  likely  to  remain  clear  and 
distinct. 

Diagnosis. — The  direct  diagnosis  of  pulmonary  stenosis  rests 
upon  these  cardinal  signs :  a  harsh  systolic  murmur,  perhaps  attended 
by  a  thrill,  in  the  pulmonic  area,  and  thence  reflected  upward  toward 
the  clavicle,  but  not  conducted  into  the  neck;  enfeeblement  of  the 
pulmonic  second  sound;  and  evidences  of  right  ventricular  hyper- 
trophy. Information  corroborative  of  this  lesion  includes,  in  con- 
genital cases  particularly,  the  presence  of  cyanosis,  dyspnea,  and 
venous  turgescence,  and,  in  numerous  other  instances,  diminished 
volume  and  increased  rate  of  the  pulse,  together  with  the  demonstra- 
tion of  a  tuberculous  infection  of  the  lungs  and  of  systemic  evi- 
dences thereof. 

Only  exceptionally  does  a  systolic  murmur  in  the  pulmonic  area 
mean  organic  stenosis  of  the  pulmonic  orifice,  for  this  "region  of 
auscultatory  romance,"  as  Balfour  so  aptly  describes  it,  is  the  site 
of  numerous  bruits,  both  functional  and  organic,  which  have  nothing 
whatever  to  do  with  a  structural  defect  of  the  right  semilunar  valve- 
cusps. 

Anemia  is  by  far  the  most  common  factor  of  a  pulmonary  systolic 
murmur,  and  a  bruit  of  this  nature  is  likely  to  be  soft  and  low-pitched, 
attended  by  a  venous  hum  in  the  neck  and -by  a  sharp  pulmonic 
second  sound,  but  unattended  by  cyanosis  and  by  hypertrophy  of 


470  PHYSICAL   DIAGNOSIS 

the  right  ventricle;  furthermore,  an  anemic  murmur  is  peculiarly 
affected  by  postural  changes,  and,  naturally,  disappears  when  the 
patient's  blood  impoverishment  improves. 

In  relative  pulmonary  stenosis,  due  to  dilatation  of  the  pulmonary 
artery,  the  pulmonic  systolic  murmur  is  more  often  soft  and  quiet 
than  loud  and  harsh,  the  right  heart  is  not  enlarged,  cyanosis  is 
wanting,  and  the  patient's  appearance  indicates  malnutrition, 
debility,  and  general  muscular  flabbiness. 

A  cardiorespiratory  murmur  is  frequently  referred  to  the  pulmonic 
area,  but  a  sound  of  this  sort  resembles  a  sudden  brief  puff  or  whiff 
of  air,  lacks  the  harmonious  vibratory  tone  of  a  genuine  bruit,  and  is 
exaggerated  by  respiratory  phases  and  by  changes  in  posture  favorable 
to  intimate  contact  between  the  heart  and  the  lung.  As  a  rule,  a 
cardiorespiratory  murmur  is  systolic,  though  it  may  be  diastolic; 
and  while  not  incompatible  with  health,  it  often  accompanies 
emphysema,  in  which  affection  both  cyanosis  and  right  ventricular 
hypertrophy  may  exist. 

The  conus  arteriosus  may  be  the  seat  of  a  systolic  bruit,  audible 
over  the  pulmonic  area,  should  this  part  of  the  right  ventricle  be 
uncovered  by  a  recession  of  the  anterior  edge  of  the  left  lung,  due, 
for  example,  to  its  deficient  inflation.  In  consequence  of  this  each 
systole  of  the  heart  thrusts  the  conus  directly  against  the  thoracic 
wall,  thereby  flattening  its  anterior  surface  and  agitating  within  the 
chamber  blood  eddies  conducted  forward  by  the  blood-current.1 
This  variety  of  murmur  usually  disappears  when  the  patient  takes  a 
deep  breath  and  holds  it,  thus  intervening  a  cushion  of  inflated  lung 
between  the  heart  and  the  chest-wall.  In  addition  to  this  point,  it 
should  be  remembered  that  a  functional  murmur  generated  within 
the  ventricular  cone  produces  no  enlargement  of  this  chamber,  nor 
is  it  attended  by  dyspnea  or  cyanosis. 

Atheroma  of  the  aortic  arch  and  true  aortic  stenosis  must  be  reckoned 
with  as  common  factors  of  a  systolic  murmur  in  the  pulmonic  area, 
but  the  murmurs  attending  both  these  lesions  are  distinctly  conducted 
into  the  carotid  arteries — a  fact  alone  sufficient  to  exclude  pulmonary 
stenosis,  though  the  differentiation  is  made  doubly  sure  by  detecting, 
in  aortic  atheroma,  left  ventricular  hypertrophy,  a  ringing  aortic 
second  sound,  and  arterial  sclerosis;  and  in  aortic  stenosis,  left 
ventricular  hypertrophy,  a  muffled  or  absent  aortic  second  sound, 
and  a  pulsus  tardus. 

The  murmur  of  mitral  re  gurgitation  may  be  clear  and  distinct  in 

1  Very  gentle  pressure  upon  the  conus  is  sufficient  to  excite  a  murmur  therein, 
as  shown  by  the  experiments  of  Thayer  and  MacCallum. 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM          '  471 

the  pulmonic  area,  but  the  mitral  murmur,  though  timed  like  that  of 
pulmonary  stenosis,  is  conducted  toward  the  left  axilla  and  supple- 
mented by  an  accentuated  pulmonic  second  sound,  and  in  cases  of 
organic  leakage,  the  left  ventricle  becomes  obviously  enlarged,  as 
well  as  the  right  side  of  the  heart. 

Aneurism  of  the  aortic  arch  is  sometimes  mistaken  for  pulmonary 
stenosis,  inasmuch  as  a  rough  systolic  murmur  and  thrill  are  common 
to  both  lesions.  If  aneurism  be  suspected,  one  should  search  for 
the  more  distinctive  signs  of  this  condition,  such  as  systolic  pulsation 
and  diastolic  shock  over  a  circumscribed  dull  area,  a  systolic 
carotid  bruit,  the  aneurismal  second  sound,  tracheal  tugging,  pulse 
inequality,  and  evidences  of  mediastinal  pressure. 

That  rare  lesion,  stenosis  of  the  pulmonary  artery,  generates  a 
murmur  indistinguishable  from  that  of  pulmonary  obstruction, 
and,  if  the  vessel  be  sufficiently  stenosed,  right  ventricular  hyper- 
trophy and  its  sequels  also  supervene.  In  venturing  to  differentiate 
these  two  conditions,  the  character  of  the  pulmonic  second  sound  is 
a  valuable  guide,  since  this  tone,  enfeebled  in  stenosis  of  the  orifice, 
is  accentuated  in  stenosis  of  the  artery,  owing  to  the  high  pressure 
therein.  The  presence  of  systolic  pulsation  at  the  sternal  end  of 
the  second  left  intercostal  space  and  impaired  resonance  in  this 
area  are  other  findings  in  favor  of  arterial  obstruction,  and  a  similar 
significance  attaches  to  the  demonstration,  in  the  upper  part  of  the 
left  lung,  of  a  cirrhotic  or  tuberculous  process  to  which  constriction 
of  the  artery  can  be  attributed. 

The  signs  of  a  perforate  interventricular  septum  are  compared  with 
those  of  a  pure  pulmonary  stenosis  on  page  475. 

PULMONARY  REGURGITATION 

Clinical  Pathology. — Leakage  at  the  pulmonic  orifice  arises 
in  consequence  of  structural  deformities  of  the  valve  or  of  undue 
stretching  of  the  muscular  sphincter,  either  of  which  defects  is 
responsible  for  faulty  approximation  of  the  valve  borders,  and  hence 
for  the  escape  of  blood  from  the  pulmonary  artery  into  the  right 
ventricle  during  its  diastole.  Pure  pulmonary  regurgitation  as  an 
isolated  lesion  is  the  rarest  variety  of  valvular  disease,  and,  in  its 
acquired  form,  is  most  commonly  met  with  in  young  adults.  Organic 
pulmonary  regurgitation  depends  upon  structural  deformities  of  the 
valve  mechanism  analogous  to  those  existing  in  aortic  regurgitation, 
these  changes  being  due  to  acute  endocarditis  more  often  arising  in 
connection  with  the  eruptive  fevers  and  septic  states  than  as  the 
result  of  rheumatism;  exceptionally  the  valve  is  damaged  by  pro- 


472  PHYSICAL   DIAGNOSIS 

giessive  sclerosis.  In  congenital  cases  fusion  of  two  of  the  valve- 
leallets  is  the  common  factor  of  the  incompetence,  and  with  this  lesion 
other  developmental  imperfections  of  the  cardiac  orifices  and  cham- 
bers are  ordinarily  associated.  Relative  pulmonary  re  gurgitation, 
due  to  dilatation  of  the  pulmonic  orifice  by  abnormally  high  pressure 
within  the  pulmonary  artery,  is  not  of  common  occurrence,  for  the 
pulmonic  ring,  being  firm  and  resistent,  only  exceptionally  stretches 
under  the  stress  of  arterial  hypertension.  When  the  orifice  enlarges 
so  as  to  allow  diastolic  leakage  of  blood  from  the  pulmonary  artery 
into  the  right  ventricle,  either  mitral  disease  or  some  indurative 
affection  of  the  lungs  should  be  looked  for  as  the  underlying  cause 
of  the  intrapulmonary  hypertension.  The  pulmonary  artery,  as 
well  as  the  orifice,  is  more  or  less  dilated  and  prone  to  undergo 
atheromatous  changes.  Exceptionally,  relative  pulmonary  regurgi- 
tation  indicates  a  purely  functional  rise  of  blood-pressure  in  the 
pulmonary  artery. 

Physical  Signs. — Inspection. — There  are  no  distinctive  visual 
signs  of  this  rare  lesion,  which,  in  its  pure,  organic  form  is  attended 
by  cough,  dyspnea,  cyanotic  pallor,  and  other  evidences  of  disordered 
pulmonary  blood-supply  and  of  arterial  anemia;  in  the  vast  majority 
of  instances  the  subject's  appearance  betrays  engorgement  of  the 
lungs  and  general  venous  stasis  incident  to  concomitant  left-sided 
valvular  defects  and  to  secondary  tricuspid  incompetence.  Systolic 
pulsation  in  the  epigastrium  and,  perhaps,  in  the  interspaces  at  the 
right  sternal  edge  is  visible  when  there  is  considerable  enlargement 
of  the  right  ventricle. 

Palpation. — Occasionally  it  is  possible  to  feel  a  basic  diastolic 
thrill,  having  its  greatest  distinctness  in  the  pulmonic  area.  Tumul- 
tuous throbbing  in  the  epigastric  region,  and,  not  infrequently,  a 
systolic,  non-expansile  hepatic  pulsation,  accompany  the  stage  of 
right  ventricular  hypertrophy. 

The  pulse  is  not  at  all  characteristic,  though,  as  a  rule,  the  radials 
are  of  small  volume,  low  tension,  and  erratic  rhythm. 

Percussion. — Cardiac  dulness  is  increased,  especially  to  the  right 
of  the  sternum,  to  an  extent  proportionate  to  the  enlargement  of  the 
right  ventricle,  and,  sooner  or  later,  right-sided  basal  impairment 
due  to  dilatation  of  the  right  auricle  supervenes.  Until  the  tension 
within  this  chamber  becomes  excessive,  there  is  no  enlargement  of 
the  hepatic  area. 

Auscultation. — Pure  pulmonary  leakage  gives  rise  to  a  soft  (rarely, 
harsh  and  rasping)  diastolic  murmur  in  the  pulmonic  area,  from 
which  point  of  greatest  intensity  the  bruit  can  be  traced  downward 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  473 

along  the  left  sternal  border  and  toward  the  apex  of  the  heart.  The 
pulmonic  second  sound  is  enfeebled  or  lost,  but  the  character  of  the 
other  cardiac  tones  undergoes  no  primary  alteration. 

Diagnosis. — A  diagnosis  of  pulmonary  regurgitation  is  justified 
by  the  following  combination  of  physical  signs :  a  diastolic  pulmonic 
murmur  conducted  down  the  sternum,  impairment  or  obliteration 
of  the  pulmonic  second  sound  without  notable  alteration  in  its  aortic 
equivalent,  right-sided  cardiac  enlargement,  and  a  frequent,  small 
arterial  pulse.  Ultimately,  to  these  findings  are  to  be  added  those 
relating  to  secondary  tricuspid  leakage  and  general  venous  engorge- 
ment. 

Relative  pulmonary  regurgitation,  of  the  type  excited  by  the  excessive 
engorgement  of  the  lungs  secondary  to  mitral  stenosis,  accounts  for 
a  diastolic  pulmonic  bruit  described  by  Steell  as  "the  murmur  of 
high  pressure  in  the  pulmonary  artery."  This  murmur  is  distin- 
guished, aside  from  its  association  with  a  primary  mitral  defect,  by 
a  most  evanescent  character,  for  the  sound  appears  and  vanishes 
according  to  pressure  variations  within  the  pulmonary  artery.  The 
pulmonic  orifice  may  be  temporarily  incompetent  in  consequence  of 
pulmonary  hypertension  induced  by  violent  exercise  and  by  deep 
breathing.  Cabot  refers  to  persons  in  perfect  health  who  were  able, 
by  prolonged  holding  of  the  breath,  to  produce  a  short,  high-pitched 
diastolic  murmur,  best  heard  in  the  second  or  third  left  interspaces, 
and  disappearing  when  respiration  was  resumed.  The  transient 
occurrence  and  the  method  of  producing  a  functional  murmur  of  this 
sort  are  sufficient  denial  of  its  organic  nature,  apart  from  the  lack  of 
consecutive  structural  changes  in  the  heart. 

Aortic  regurgitation  can  beget  a  soft  diastolic  bruit  having  great 
intensity  in  the  pulmonic  area,  and  thence  propagated  downward 
like  the  murmur  of  pulmonary  regurgitation.  Corrigan's  disease, 
however,  is  accompanied "  by  an  ox-heart,  throbbing  arteries,  the 
water-hammer  pulse,  an  obscure  aortic,  and  a  sharp  pulmonic, 
second  sound;  while  pulmonary  regurgitation  is  associated  with 
right  ventricular  enlargement,  quiet  arteries,  a  small  pulse,  a  feeble 
pulmonic,  and  unimpaired  aortic,  second  sound. 

CONGENITAL  CARDIAC  DISEASE 

Clinical  Pathology. — Of  the  numerous  forms  of  congenital  heart 
disease,  pulmonary  stenosis,  defects  of  the  interventricular  septum, 
and  patency  of  the  duttus  arteriosus  are  of  clinical  interest,  owing  to 
their  relative  frequency  as  antenatal  lesions  and  because  they  offer, 


474 


PHYSICAL   DIAGNOSIS 


when  existing  singly,  reasonably  good  opportunities  for  a  diagnosis 
during  life.  Of  purely  pathologic  interest  are  the  structural  changes 
relating  to  a  patent  foramen  ovale  (Fig.  181),  and  to  absence  oj  the 
septa  between  the  auricles,  the  ventricles,  or  both.  Congenital 
lesions  of  the  tricuspid,  mitral,  and  aortic  valves  have  been  suffi- 
ciently discussed  under  Valvular  Disease. 

Congenital  malposition  of  the  heart  may  take  the  form  of  dextro- 
cardia,  in  which  condition  the  heart  lies  on  the  right  side  of  the 
thorax,  thus  giving  a  "mirror  picture"  of  the  normal  physical  signs, 


Right  auricular  wall 


—  Right  ventricle 


Fig.  181. — Patent  foramen  ovale  (Philadelphia  General  Hospital). 

and  in  this  anomaly  there  is  generally  a  corresponding  transposition 
of  the  abdominal  viscera,  the  combined  abdominothoracic  dislocation 
constituting  a  situs  viscerum  inversus.  Persistence  of  the  heart  in 
its  normal  fetal  position  in  the  median  line  of  the  thorax  is  known 
as  mesocardia.  Ectopia  cordis,  or  the  situation  of  the  heart  outside 
the  thorax,  occurs  in  three  forms:  pectoralis,  in  which  the  heart, 
covered  by  the  pericardium  and  integument  or  by  the  pericardium 
only,  bulges  through  a  midsternal  fissure;  cervicalis,  or  a  displacement 
of  the  heart  upward  into  the  neck  close  to  the  lower  jaw;  and 
abdominalis,  or  subphrenic  displacement  of  the  heart  downward  into 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM  475 

the  abdominal  cavity.  The  last  of  these  anomalies  is  not  necessarily 
incompatible  with  many  years  of  life,  but  in  the  other  two  postnatal 
existence,  if  at  all  possible,  is  of  brief  duration. 

Anomalies  of  size  comprise  congenital  hypertrophy  and  atrophy, 
the  former  ordinarily  being  the  result  of  fetal  endocarditis,  and  the 
latter  part  and  parcel  of  a  general  cardiovascular  hypoplasia  some- 
times incident  to  chlorosis  and  to  lymphatism. 

Transposition  of  the  aorta  and  pulmonary  artery,  the  former  having 
a  right,  and  the  latter  a  left,  ventricular  origin,  is  a  peculiarity  of 
development  commonly  associated  with  a  persistent  arterial  duct 
between  the  two  transposed  arterial  channels.  Communication  of 
both  aorta  and  pulmonary  artery  with  the  same  ventricle,  with  or 
without  malformation  of  the  septa  and  the  duct  of  Botallo,  is  a  type 
of  anomaly  somewhat  more  common  than  the  foregoing. 

Physical  Signs. — Congenital  pulmonary  stenosis,  like  the  acquired 
form,  generates  a  systolic  murmur  most  intense  in  the  pulmonic 
area,  and  thence  transmitted  toward  the  left  clavicle,  but  not  into  the 
neck,  of  which  leading  sign  a  systolic  basic  thrill  and  hypertrophy  of 
the  right  ventricle  are  strongly  confirmatory.  (See  p.  467.) 

A  pervious  interventricular  septum  is  commonly  combined  with 
the  foregoing  lesion,  and  in  this  event  its  auscultatory  signs  are  usually 
so  overshadowed  by  the  pulmonary  murmur  as  to  render  it  unrecogni- 
zable. An  isolated  septal  perforation  may  be  identified  by  finding 
a  loud  and  harsh  systolic  bruit  with  its  punctum  maximum  in  the 
fourth  left  interspace,  between  the  sternum  and  the  midclavicular  line, 
and  highly  characteristic  in  that  it  is  a  continuous  sound  running 
through  the  entire  cardiac  cycle  (Rogers'  murmur).  A  systolic 
thrill  is  not  uncommonly  palpable.  During  systole  the  intensity 
of  this  murmur  is  increased  and  the  pitch  raised,  while  with  diastole 
it  dwindles  to  a  low,  though  distinct,  rumble.  The  bruit  has  been 
likened  to  the  rasping  sound  of  a  grinder's  wheel  when  a  knife  is 
being  sharpened.  Hypertrophy  of  the  right  ventricle  is  the 
ordinary  consequence  of  this  defect,  which,  save  for  the  absence  of 
pulmonary  congestion,  accounts  for  objective  phenomena  like  those 
of  mitral  stenosis. 

Persistence  of  the  ductus  arteriosus  has  been  recognized  during  life 
by  the  detection  of  a  late  systolic  murmur,  audible  in  the  pulmonic 
area,  and  propagated  toward  the  apex.  This  murmur,  which  appears 
immediately  to  follow,  rather  than  exactly  to  coincide  with,  the  first 
sound,  is  generally  distinguished  by  a  high  pitch,  by  considerable 
intensity  (especially  during  inspiration),  and  by  prolonged  duration. 
Accentuation  of  the  pulmonic  second  sound  and  the  presence  of 
right  ventricular  hypertrophy  are  important  secondary  signs,  while 


476  PHYSICAL   DIAGNOSIS 

paradoxic  weakening  of  the  pulse  during  inspiration,  and  systolic  pul- 
sation in  the  second  left  interspace  also  have  been  observed. 

Patent  foramen  ovale,  if  an  isolated  lesion,  may  be  wholly  symp- 
tomless;  under  no  circumstance  does  a  pervious  interauricular 
septum  give  rise  to  a  distinctive  clinical  picture. 

Diagnosis. — Congenital  disease  of  the  heart  is  indicated  by  a 
history  of  cyanosis  from  birth, — a  "blue  baby,"  in  lay  vernacular, — 
with  dyspnea  and  physical  blemishes,  such  as  dwarfed  stature 
and  clubbed  fingers  and  toes.  As  a  rule,  physical  exertion  de- 
cidedly deepens  the  blueness.  Given  these  general  indications,  the 
discovery  of  one  of  the  above  groups  of  signs  may  lead  to  the 
diagnosis  of  the  precise  defect.  The  very  name,  morbus  ccerideus, 
applied  to  congenital  heart  lesions  as  a  class,  denotes  the  im- 
portance of  cyanosis  as  a  sign  of  these  affections.  It  probably 
means  imperfect  aeration  of  the  blood,  despite  attempts  made  to 
attribute  it  chiefly  to  venous  stasis  and  to  commingling  of  the 
arterial  and  venous  currents.  Cyanosis  is  most  common  and 
usually  most  striking  in  pulmonary  stenosis,  but  it  is  by  no  means 
restricted  to  this  lesion,  and  this  is  likewise  true  of  the  other  signs 
just  noted. 

ANEURISM  OF  THE  AORTA 
ANEURISM   OF  THE   THORACIC  AORTA 

Clinical  Pathology. — Atheroma  of  the  aorta  and  high  blood-pres- 
sure are  the  almost  invariable  essential  factors  of  aneurism  of  the 
thoracic  aorta,  which  is  prone  to  occur  in  men  during  the  third  and 
fourth  decades  of  life,  when,  as  Coats  expresses  it,  "the  period  of 
greatest  bodily  vigor  overlaps  the  period  of  beginning  atheroma." 
In  other  words,  the  lesion  develops  most  commonly  at  that  time  of 
life  when  the  cardiac  force  is  greatest,  while  the  vessel  is  impaired 
by  a  degenerative  process,  which,  being  incipient  and,  therefore, 
unattended  by  compensatory  endarteritis,  damages  without  attempt- 
ing to  repair  its  inroads.  Syphilis  is  by  far  the  commonest  cause  of 
the  arterial  degeneration,  though  bacterial  toxins,  infected  emboli, 
plumbism,  gout,  and  alcohol  are  also  accredited  factors  of  sclerosis 
whereby  the  artery  is  likely  to  yield,  either  gradually  under  the  tax 
of  persistently  high  blood-pressure,  or  suddenly  in  consequence  of 
a  violent  muscular  strain,  as  from  lifting  a  heavy  weight  or  from  a 
hard  fit  of  coughing.  Under  these  conditions  one  or  more  of  the 
impaired  arterial  coats  may  give  way  at  the  site  of  a  focal  or  circum- 
scribed atheroma,  with  subsequent  pouch-like  bulging  of  the  arterial 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM 


477 


wall  and  the  formation  of  a  saccular  aneurism.  In  diffuse,  fusiform 
aortic  aneurism  wide-spread  atheromatous  enfeeblement  of  the 
vessel-wall,  without  especially  vulnerable  local  patches  of  degenera- 
tion, is  to  be  assumed. 

Of  all  cases  of  aortic  aneurism,  approximately  three-fourths  affect 
the  thoracic  division,  the  favorite  site  being  the  ascending  portion  of  the 
arch,  after  which,  in  order  of  incidence,  the  transverse  and  descending 
portions,  and  the  descending  thoracic  aorta  are  implicated  (Fig.  182). 
Saccular  aneurism  produces  the  clearest  physical  signs,  and  is  by 
far  the  most  Common  type  met  with  clinically,  this  variety  constituting 
about  95  per  cent,  of  the  570  cases  of  thoracic  aneurism  collected  by 


I.  Ascending  arch 


III.  Transverse  arch 

IV.  Descending  arch 


V.  Descending  thoracic 
aorta 


II.  Abdominal  aorta 


Fig.  182. — Relative  site  incidence  of  aortic  aneurism. 

Hare  and  Holder.  Fusiform  aneurismal  dilatation  of  the  aorta 
(Fig.  184)  may  attain  a  huge  size  without  attracting  attention.  As 
a  rule,  there  is  but  a  single  sac,  which  may  be  as  small  as  a  marble 
or  as  large  as  a  football;  exceptionally,  the  aorta  is  found  to  be 
studded  with  multiple  sacculations.  The  changes  in  the  wall  of  the 
aneurism  comprise  thinning  and  ultimate  disappearance  of  the  media 
from  atrophy  and  destruction  of  the  muscular  and  elastic  fibers, 
and,  subsequently,  fibrous  thickening  of  the  intima  and  adventitia, 
the  latter  coat  virtually  forming  the  wall  of  the  sac  and  frequently 
being  matted  by  adhesions  to  neighboring  structures.  Eventually 


478 


PHYSICAL    DIAGNOSIS 


every  vestige  of  the  three  arterial  coats  may  disappear  and  a  sac 
be  constructed  of  the  surrounding  tissues— -false  aneurism,  in  con- 
trast to  a  true  aneurism,  in  which  at  least  one  arterial  coat  persists. 
Or,  a  dissecting  aneurism  may  arise,  should  a  breach  be  torn  in  the 
intima  through  which  the  blood  penetrates  to  bore  a  channel 
between  the  outer  coats  of  the  vessel;  and  if  such  a  channel. 


Aneurismal  sac 


Innominate  artery 

Left  common  carotid 
artery 


Left  subclavian  artery 


Descending  aortic  arcb 


Ascending  aortic  arch 
Pulmonary  artery 


Conus  arteriosus 


Right  ventricle 


Fig.  183. — Saccular  aneurism  of  the  aortic  arch  (Philadelphia  General  Hospital). 

instead  of  draining  into  the  surrounding  parts,  leads  back  into  the 
aorta  by  another  opening  in  the  intima,  the  curious  anomaly  termed 
double  aorta  is  formed.  An  arteriovenous  aneurism,  effecting  chiefly 
the  peripheral  vessels  (Fig.  185),  consists  of  an  abnormal  com- 
munication between  an  artery  and  a  vein,  the  connection  between 
the  two  vessels  being  either  direct  (aneurismal  varix)  or  established 


DISEASES   OF   THE   CARDIOVASCULAR   SYSTEM 


479 


by  an  intervening  sac  (varicose  aneurism).  A  laminated  fibrinous 
clot  usually  occupies  the  interior  of  the  aneurismal  sac,  which, 
indeed,  may  be  wholly  obliterated  thereby,  though  rupture  of  the 
sac  is  the  ordinary  termination.  This  occurs  most  frequently  into 
the  left  pleural  cavity,  and  then,  in  this  order  of  incidence,  into 
the  pericardium,  right  pleura,  esophagus,  and  larger  air-passages; 
less  commonly  the  superior  vena  cava,  the  pulmonary  artery,  or 
the  heart  is  penetrated,  or  the  rupture  may  be  external. 


Trachea 


Focus  of  soften- 
ing 


Ascending  aorti 

arch 
Pulmonary 

artery 
Right  auricl 


Right  ventricle 


Left  common 
carotid  artery 

Left  subclavian 
artery 


Aneurismal  sac 


Focus  of 
softening 


Left  auricle 


Left  ventricle 


Fig.  184. — Fusiform  aneurism  of  the  aortic  arch  (Jefferson  Hospital  Laboratories). 

Some  aneurisms  remain  symptomatically  latent  for  a  long  period, 
but  ordinarily  the  enlarging  sac  encroaches  upon  the  surrounding 
structures,  displacing  them  and  exciting  therein  various  mechanical, 
inflammatory,  and  necrotic  changes,  due  to  compression.  The 
bronchi  and  lungs  are  particularly  liable  to  damage  thus  inflicted., 
which  takes  the  form  of  bronchial  ulceration,  necrosis,  stenosis,  and 
ectasis,  and  of  pneumonic,  fibroid,  and  gangrenous  processes  in  the 


480 


PHYSICAL   DIAGNOSIS 


lungs;  erosion  of  the  bony  thorax — ribs,  sternum,  vertebrae — is  not 
uncommon;  and  pressure  phenomena  relating  to  the  gullet  and  to 
the  nerves  and  great  vessels  of  the  mediastinum  are  familiar  findings. 
Aortic  aneurism  is  commonly  attended  by  cardiac  hypertrophy,  but 
it  is  questionable  if  the  aneurism,  per  se,  is  the  primary  factor  of  the 
enlarged  heart. 

The  study  of  thoracic  aneurism  is  facilitated  by  localizing  the 
lesion  to  some  one  of  the  following  four  clinical  divisions  of  the 

artery:  (a)  ascending  arch,  or  that  por- 
tion of  the  vessel  extending  from  the 
base  of  the  left  ventricle  to  the  orifice 
of  the  innominate  artery,  and  corre- 
sponding to  the  two  anatomic  portions 
termed  the  ascending  aorta  and  the 
first  part  of  the  aortic  arch ;  (b)  trans- 
verse arch,  between  the  innominate  and 
the  left  subclavian  arteries  and  includ- 
ing their  mouths;  (c)  descending  arch, 
lying  between  the  left  subclavian  and 
the  fourth  thoracic  vertebra;  (d)  de- 
scending thoracic  aorta,  occupying  the 
posterior  mediastinum  between  the 
fourth  thoracic  vertebra  and  the  aortic 
opening  in  the  diaphragm  at  the  level 
of  the  twelfth  thoracic  vertebra.  The 
surface  topography  of  the  thoracic 
aorta  has  been  given  on  page  311. 

Aneurisms  of  the  ascending  aortic  arch 
usually  arise  from  the  convexity  of  the 
vessel  above  the  pericardial  limit,  and 
pass  forward  and  to  the  right,  appear- 
ing in  the  neighborhood  of  the  second 
and  third  right  intercostal  spaces  and 
the  sternum  (Fig.  187),  or  they  affect 
the  concavity  of  the  aorta,  and  give  rise 
to  physical  signs  along  the  left  sternal 
border.  Or  the  dilatation  may  be  intra- 
pericardial,  arising  at  or  immediately  above  the  sinuses  of  Valsalva, 
in  which  case  rupture  into  the  pericardium,  causing  instant  death,  is 
probable  before  the  aneurism  reaches  a  large  size.  Aneurisms  of 
the  ascending  arch  tend  to  cause  striking  cardiac  displacement, 
to  stretch  the  aortic  ring  so  as  to  set  up  relative  aortic  leakage,  and 


Fig.  185. — Arteriovenous  aneur- 
ism (Jefferson  Hospital). 


DISEASES   OF   THE   CARDIOVASCULAR   SYSTEM  481 

to  compress  the  superior  (rarely,  the  inferior)  vena  cava,  the  sub- 
clavian  vessels,  the  pulmonary  artery,  and  the  right  recurrent  laryn- 
geal  nerve.  Rupture  may  take  place  into  the  right  pleura,  the 
pericardium,  or,  exceptionally,  into  the  superior  vena  cava. 

Aneurisms  of  the  transverse  arch  commonly  spring  from  the  pos- 
terior wall  of  the  aorta,  and  are  more  likely  to  extend  backward 
toward  the  spine  or  to  invade  the  pleurae,  than  to  press  forward  and 
erode  the  chest-wall  beneath  or  alongside  the  sternum.  Implication 
of  both  the  ascending  and  transverse  portions,  which  sometimes 
occurs,  results  in  a  tumor  of  extraordinary  dimensions  whose  exten- 
sion takes  an  upward  and  outward  direction  (Fig.  188).  The  struc- 
tures particularly  exposed  to  compression  by  an  aneurism  of  the 
transverse  arch  are  the  trachea,  esophagus,  left  bronchus,  and  left 
recurrent  laryngeal  nerve,  and,  less  frequently,  the  sympathetic  nerve 
and  the  thoracic  duct.  When  the  sac  compresses,  communicates 
with,  or  lies  between  the  innominate,  left  common  carotid,  or  left 
subclavian  arteries,  corresponding  alterations  take  place  in  the  carotid 
and  radial  pulses  (q.  v.).  The  potential  causes  of  death  in  this  type 
of  aneurism  include  pressure-asphyxia,  secondary  pulmonary  com- 
plications, and  hemorrhage  from  rupture  of  the  sac  into  the  trachea, 
left  bronchus,  pleurae,  or  posterior  mediastinal  space. 

Aneurisms  of  the  descending  arch  extend  to  the  left  and  backward, 
and  if  they  reach  the  surface,  appear  alongside  the  spine  in  the  left 
interscapular  region.  The  accompanying  illustration  (Fig.  189) 
shows  the  conspicuous  deformity  produced  by  such  a  tumor,  which, 
owing  to  its  deep  situation,  must  attain  an  enormous  size  to  cause 
surface  signs.  Nor  are  evidences  of  intrathoracic  pressure  well 
denned  in  the  average  case;  the  structures  most  likely  thus  to  suffer 
are  the  esophagus,  the  thoracic  duct,  the  spinal  nerves,  and  the 
vertebrae,  while  less  commonly  the  root  of  the  left  lung  is  compressed. 
Rupture  into  the  esophagus,  left  pleural  sac,  or  left  bronchus,  and 
consecutive  lesions  of  the  lungs  are  the  ordinary  causes  of  death  in 
aneurism  of  this  portion  of  the  aortic  arch. 

Aneurisms  of  the  descending  thoracic  aorta,  usually  situated  just 
above  the  diaphragm,  lie  to  the  left  or  in  front  of  the  lower  thoracic 
vertebrae  and  in  close  contact  therewith.  Pressure-erosion  of  these 
bones,  irritation  of  the  spinal  nerves,  and  perhaps  compression  of 
the  esophagus  and  pleuropulmonary  tissues  are  to  be  looked  for 
when  the  aneurism  does  not  follow  a  latent  course.  Death  by  rupture 
of  the  sac  into  the  pleura  or  the  esophagus  is  the  usual  outcome  of  an 
aneurismal  dilatation  in  this  situation. 

Physical  Signs. — Inspection. — The  chest-wall  should  be  carefully 
31 


482 


PHYSICAL   DIAGNOSIS 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM 


483 


scrutinized  with  the  object  of  finding  an  area  of  abnormal  systolic 
pulsation,  which  is  always  highly  suggestive  of  aneurism.  The  favorite 
sites  of  such  pulsations  are  the  anterior  surface  of  the  thorax,  between 
the  clavicle  and  the  third  rib,  near  the  sternal  border,  especially  on  the 
right  side  (ascending  arch) ,  the  suprasternal  notch  and  the  right  supra- 
clavicular  space  (transverse  arch;  innominate  artery),  and  the  left 
interscapular  region  near  the  spine  (descending  arch) .  Feeble  pulsa- 
tions— and  these  are  by  no  means  exceptional — are  usually  discovered 
only  by  most  minute  inspection  of  the  questionable  area  from  an 
oblique  viewpoint;  or  by  laying  the  finger-tips  over  the  part  and  noting 


Fig.  187. — Aneurism  of  the  ascending  aortic  arch  (Jefferson  Hospital). 

their  rhythmic  elevation  with  each  beat  of  the  heart;  or  by  observing 
that  the  barrel  of  a  single  stethoscope,  whose  chest-piece  is  applied 
to  an  interspace,  is  periodically  tilted  by  a  transmitted  throb  from 
beneath.  On  the  other  hand,  sometimes  the  impulses  are  so  strong  as 
to  cause  an  extensive  circumscribed  heaving  of  the  chest-wall,  appar- 
ent at  first  glance.  According  to  the  amount  of  erosion  produced,  a 
local  bulging  or  even  a  definite  tumor,  each  pulsatile,  may  appear, 
and  over  the  swelling  the  tissues  tend  to  become  brawny,  edematous, 
and  stained  purple  or  black  with  suffused  blood,  while  later  the  sur- 
face structures  may  break  down  and  a  mixture  of  serum  and  blood 


484 


PHYSICAL   DIAGNOSIS 


trickle  from  the  sac.  Figs.  187,  188,  and  189  show  the  deformities 
produced  by  large  aneurismal  tumors  which  have  eroded  the  chest- 
wall.  The  cardiac  apex  is  crowded  below  and  outside  its  normal 
site,  and  may  beat  tumultuously,  owing  to  concomitant  hypertrophy. 
Engorged  veins  upon  the  chest  and  upper  extremities,  edema  of  one 
arm,  cyanosis,  dyspnea,  unequal  pupils,  and  unilateral  sweating  are 

other  objective  phenomena 
whose  prominence  depends 
upon  the  degree  and  situation 
of  the  mediastinal  pressure  in 
the  individual  case.  Signorelli 
attaches  importance  to  wast- 
ing of  the  left  sternomastoid 
muscle  as  a  sign  (due  to  nerve 
degeneration  from  pressure) 
of  aneurism  of  the  transverse 
and  descending  arch.  The 
larynx  may  be  immobilized, 
depressed,  and  displaced  to- 
ward the  left  by  a  large  an- 
eurism of  the  ascending  part 
of  the  aortic  arch.  (Boinet.) 
X-ray  examination  with  the 
fluoroscope  is  a  great  diag- 
nostic aid,  for  it  may  clearly 
reveal  a  shadow  to  the  right, 
to  the  left,  or  on  both  sides  of 
the  sternum  in  aneurism  of 
the  aortic  arch,  and  in  aneur- 
ism of  the  descending  tho- 
racic aorta  this  method  of  ex- 
amination often  is  the  only 
means  of  securing  definite  data.  Moreover,  the  *-rays  show  the 
extent  of  the  cardiac  dislocation  consequent  to  pressure  by  the 
tumor,  and,  if  the  sac  be  resilient  and  comparatively  clot-free, 
expansile  pulsations  are  unmistakably  shadowed  upon  the  fluo- 
rescent screen. 

Palpation— -The  extent  and  character  of  the  pulsation  are  best 
judged  by  palpation,  which  also  may  discover  an  abnormal  throb  too 
feeble  to  attract  the  eye.  The  palm  of  the  hand  appreciates  either 
an  obscure  indefinite  pulsation  or  a  powerful  lifting  or  heaving  impact 
over  the  aneurism,  according  to  its  size  and  distance  from  the  chest- 


Fig.  1 88. — Aneurism  of  the  ascending 
and  transverse  aortic  arch  and  innominate 
artery  (Jefferson  Hospital). 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM 


485 


wall.  If  the  latter  be  eroded,  so  that  the  sac  projects  externally 
as  a  tumor,  a  trio  of  valuable  signs  becomes  available — expansile 
pulsation,  diastolic  shock,  and  systolic  thrill.  The  expansile  pulsa- 
tion is  due  to  the  uniform  distention  of  the  sac  with  blood,  and  the 
sharp,  short  diastolic  shock  immediately  following  is  produced  by  the 
sudden  recoil  of  the  aortic  wall  after  its  systolic  distention.  The 
thrill  often  associated  with  these  two  signs  corresponds  to  systole  and 
has  a  peculiar  vibratory  quality.  The  foregoing  findings,  practi- 
cally pathognomonic  of  aneurism,  indicate  a  resilient  sac  having  com- 
paratively fluid  contents,  and  a  tumor  of  this  sort  is  not  unlikely  to 
be  so  soft  and  fluctuating  that  any  manipulation,  save  the  gentlest, 


Aneurismal  tumor 
Displaced  left  scapula 


Fig.  189. — Aneurism  of  the  descending  aortic  arch  (Jefferson  Hospital). 

is  interdicted,  for  fear  of  rupturing  the  fragile  wall.  These  signs, 
of  course,  are  not  found  over  an  aneurismal  tumor  having  a  rigid, 
thick  wall,  reinforced  by  a  laminated  clot  so  large  and  firm  as  to 
interfere  with  the  generation  and  conduction  of  vibrations  and  to 
impair  the  sac's  mural  elasticity.  When  these  conditions  rule,  the 


486 


PHYSICAL    DIAGNOSIS 


consistence  of  the  tumor  will  be  firm  and  hard,  and  its  pulsation  a 
lifting  impact.  Tracheal  tugging,  though  presumptive  evidence  of 
aneurism,  especially  of  the  transverse  arch,  is  not  distinctive,  for 
a  similar  systolic  depression  of  the  windpipe  is  sometimes  seen  in 
simple  dilatation  of  the  aorta  and  in  mediastinal  neoplasm.  (See 
p.  328.)  An  inversion  of  Oliver's  sign,  or  a  rhythmic  elevation  of 
the  trachea  with  systole,  has  been  described  by  Hirtz  in  aneurism 
springing  from  the  convexity  of  the  aortic  arch.  Aside  from  the 
spontaneous  pain  the  patient  suffers,  local  tenderness  and  sometimes 
excruciating  radiations  of  pain  are  commonly  provoked  by  pressure 
over  the  site  of  the  aneurism:  when,  for  example,  the  descending 
arch  is  implicated,  tapping  the  upper  thoracic  vertebrae  sets  up 
aching  of  the  spine  and  acute  lancinating  pain  radiating  thence  over 
the  left  side  of  the  thorax. 

The  pulse  in  the  radial  and  carotid  arteries  is  significantly  modified 
by  aneurisms  of  the  ascending  and  transverse  portions  of  the  aortic 
arch,  the  nature  of  these  alterations  corresponding  essentially  to  the 
situation  of  the  sac.  Aneurism  of  the  ascending  arch,  situated  between 
the  aortic  orifice  and  the  innominate  artery,  but  not  compressing  the 


Fig.  190. — Synchronous  sphygmographic  tracings  of  the  right  and  the  left  carotid 
arteries  in  a  case  of  innominate  aneurism.     (Tracing  by  Dr.  G.  Bachmann.) 

latter,  obviously  modifies  both  radials  identically,  and  under  this  cir- 
cumstance the  right  and  left  pulses  at  the  wrist  are  perfectly  synchro- 
nous and  equal,  though  they  are  both  likely  to  be  delayed  in  comparison 
with  the  precordial  impulse,  and  unnaturally  full  between  beats, 
while  the  pulse- waves  are  of  moderate  amplitude,  prolonged  duration, 
and  deliberate  subsidence.  Inequality  in  the  time,  volume,  and  ten- 
sion of  the  two  radial  pulses  suggests  pressure  upon,  or  obstruction 
within,  either  the  innominate  artery  or  the  left  subclavian  artery  by 


DISEASES    OF    THE    CARDIOVASCULAR    SYSTEM 


487 


an  aneurism  attached  to  some  part  of  the  transverse  arch.  If  the 
innominate  be  obstructed  or  compressed  by  an  aneurism  lying 
between  the  orifice  of  this  trunk  and  the  left  subclavian,  the  right 
radial  pulse  will  be  later,  smaller,  weaker,  and  softer  than  the  left. 
If  the  left  subclavian  artery  leads  directly  from  an  aneurismal  sac, 
or  if  it  be  compressed  by  a  dilatation  of  the  transverse  arch  well  to 
the  left  of  the  innominate's  origin,  the  left  radial  pulse  will  exhibit  the 
alterations  just  noted.  The  sphygmogram  reproduced  above  graphic- 
ally illustrates  these  pulse  differences,  so  suggestive  of  aneurismal 
pressure  (Fig.  191).  Pulse  changes  in  the  carotid  arteries  like 
those  affecting  the  radials  also  occur,  inasmuch  as  innominate 
obstruction  must  check  and  diminish  the  current  within  the  right 
common  carotid  and  its  branches,  while  factors  acting  on  the  left 
subclavian  artery  must  similarly  affect  the  adjacent  left  com- 
mon carotid.  It  is  quite  apparent  that  an  aortic  aneurism  distal 
to  and  well  removed  from  the  left  subclavian  artery  cannot  influence 
the  pulses  in  the  arms  and  wrists,  though  both  femoral  beats  may  be 


Fig.   19 1. — Simultaneous  sphygmographic  tracings  of  the   carotid  artery  and  of  an 
aortic  aneurismal  sac.    (Tracing  by  Dr.  G.  Bachmann.) 

enfeebled  and  delayed,  yet  synchronous.  Osier  noted  complete 
abolition  of  pulsation  in  the  abdominal  aorta  in  aneurism  of  the 
descending  arch.  In  addition  to  noting  the  above  important  pulse 
deviations,  one  should  not  fail  to  study  the  condition  of  the  arterial 


488  PHYSICAL   DIAGNOSIS 

walls,  inasmuch  as  arteriosclerosis  of  the  peripheral  vessels  is  in 
favor  of  aneurism. 

Percussion. — As  an  aneurism  approaches  the  chest-wall  percussion 
resonance  is  thereby  impaired  over  an  area  corresponding  to  the  site 
of  the  sac.  Percussion  is  of  unquestionable  value  in  recognizing  a 
beginning  aneurismal  enlargement  of  the  ascending  and  transverse 
arch,  in  which  an  unnaturally  broad  zone  of  supracardiac  vascular 
dulness,  with  proportionately  increased  tactile  resistance,  is  frequently 
appreciable  long  before  other  physical  signs  appear.  Later,  as  the 
sac  enlarges,  frank  dulness,  or  even  flatness,  becomes  well  marked 
over  and  alongside  the  manubrium,  in  aneurisms  of  the  ascending 
and  transverse  portions;  and  in  the  left  interscapular  region,  near 
the  spine,  when  the  descending  arch  is  greatly  dilated.  Obviously, 
a  small  intrapericardial  aneurism  lies  beyond  the  range  of  per- 
cussion, and  the  same  is  true  of  an  aneurism  of  the  descending 
thoracic  aorta,  unless  it  be  of  great  size. 

Auscultation. — The  presence  or  absence  of  a  murmur  over  an 
aneurism  is  of  very  minor  import,  for  it  occurs  with  great  inconstancy 
and  is  in  no  wise  distinctive.  A  systolic  bruit  may  be  generated 
within  an  aneurismal  sac,  or  within  the  aorta  lying  beyond  and 
compressed  by  the  dilatation  (Fig.  163,  p.  393);  and  in  some  cases 
a  precisely  similar  murmur  arises  at  a  stenotic  aortic  orifice, 
and  is  transmitted  thence  into  the  sac  and  through  the  aorta. 
Here  may  be  mentioned  Drummond's  sign:  a  rhythmic  systolic 
whiff  sometimes  heard  at  the  open  mouth  of  a  subject  of  aortic 
aneurism ;  Sansom's  sign :  a  similar  sound,  audible  with  a  steth- 
oscope applied  to  the  patient's  lips;  and  Glasgow's  sign:  a  systolic 
sound  heard  over  the  brachial  artery.  The  foregoing  oral  signs 
must  not  be  confused  with  Galvagni's  buccal  souffle:  rhythmic  sys- 
tolic interruption  of  the  expiratory  sound  audible  at  the  subject's 
mouth,  in  paracardial  pleurisy  and  in  dilated  hypertrophy  of  the 
heart,  and  attributed  to  the  rush  of  intrapulmonary  air  columns 
expelled  by  the  impact  of  the  heart. 

The  most  valuable  auscultatory  sign  of  aneurism  is  an  intense  and 
low-pitched  diastolic  sound  over  the  aortic  area,  and  usually  audible 
for  a  considerable  distance  on  both  sides  of  the  sternum,  This 
distinctive  sound  is  exactly  synchronous  with  the  palpable  diastolic 
shock,  and  is  probably  due  not  so  much  to  the  snap  of  the  aortic 
cusps,  as  to  sudden  tension  of  the  aortic  wall.  A  diastolic  murmur 
of  associated  aortic  regurgitation  is  frequently  also  audible,  but 
despite  this  the  aneurismal  second  sound  usually  persists,  though 
it  is  modified  by  the  attendant  bruit. 


DISEASES    OF   THE    CARDIOVASCULAR    SYSTEM  489 

Over  the  sternum  loud  tubular  breathing  is  heard  should  the 
tracheal  breath-sounds  be  conducted  to  the  surface  by  an  aneur- 
ism adjacent  to  the  wind-pipe,  while  noisy  and  stridulous  breathing 
may  mean  either  stenosis  of  one  of  the  larger  air-passages  or 
pressure  paralysis  of  the  recurrent  laryngeal  nerve.  In  some 
instances  examination  of  the  chest  gives  positive  evidence  of  pul- 
monary atelectasis,  consolidation  and  congestion,  and  of  pleural 
effusion  symptomatic  of  pressure  upon  a  bronchus,  the  pulmonary 
tissue,  the  pulmonary  veins,  and  the  azygos  veins,  respectively. 

Diagnosis. — Increase  in  the  transverse  vessel  dulness  and  a 
barely  palpable  systolic  pulsation  at  the  level  of  the  second  inter- 
space in  a  hard-working  man  with  rigid  arteries,  and  who  con- 
fesses to  syphilis  or  whose  blood  affords  a  positive  Wassermann 
reaction,  are  highly  suggestive  of  beginning  aneurismal  dilatation 
of  the  first  or  second  divisions  of  the  aortic  arch — this,  despite  no 
murmur,  thrill,  tumor,  nor  pressure  symptoms.  In  a  case  of  this 
sort  the  #-ray  sometimes  furnishes  invaluable  positive  evidence. 
At  a  later  stage,  when  the  aneurism  nears  the  surface  or  erodes  it, 
an  area  of  circumscribed  dulness  or  a  definite  tumor,  heaving  or 
expansile  pulsation,  a  diastolic  shock,  the  aneurismal  second  sound, 
the  tracheal  tug,  a  thrill,  and  a  systolic  murmur  complete  the  clinical 
picture.  Not  only  may  the  pulses  of  the  two  sides  differ  in  time  and 
in  volume,  but  not  infrequently,  according  to  Williamson,  there  is 
a  difference  of  from  20  to  30  mm.  in  the  blood-pressure  of  the  right 
and  left  peripheral  pulses.  The  pupil  on  the  side  of  the  lower 
pressure  is  the  larger,  MacKinnon  has  found. 

Pressure  symptoms  corroborative  of  these  physical  signs,  and, 
indeed,  in  some  instances  the  sole  evidence  of  the  lesion,  are  much 
more  conspicuous  in  aneurism  of  the  transverse  and  descending 
portions  of  the  arch  than  in  aneurism  of  the  ascending  part,  a  fact 
that  prompted  the  elder  Broadbent  to  term  the  former  the 
" aneurism  of  symptoms"  and  the  latter  the  "aneurism  of  physical 
signs."  The  pertinent  symptoms  due  to  pressure  vary  with  the  site 
of  the  compression,  but  a  general  summary  of  such  effects  may  be 
expressed  as  follows:  (a)  pain,  of  boring,  anginose,  or  radiating 
character;  (6)  dyspnea  and  dysphagia;  (<:)  cough,  bloody  expectora- 
tion, huskiness,  brassy  voice,  aphonia,  and  stridor;  (d)  inequality 
of  the  pupils,  unilateral  sweating,  hyperemia,  and  pallor  of  the 
face;  (e)  engorgement  of  the  superficial  veins,  with  edema  and  suf- 
fusion of  the  upper  extremities,  neck,  and  face;  and  (/)  the  second- 
ary lesions  of  the  bronchopulmonary  system  referred  to  above. 
Hoesslm  has  noted  stridulous  expiration  interrupted  during  dias- 


49°  PHYSICAL    DIAGNOSIS 

tole  as  a  result  of  pressure  upon  the  trachea  by  an  aneurismal 
growth. 

Rupture  of  an  aortic  aneurism  into  the  superior  -vena  cava,  forming 
an  arteriovenous  aneurism,  is  betrayed  by  the  abrupt  onset  of  urgent 
dyspnea,  extreme  engorgement  of  the  cervical  veins,  and  cyanosis 
and  edema  of  the  face  and  neck.  These  signs  persist,  should  the 
subject  live,  and  later  the  chest  and  upper  extremities  are  disfigured 
by  a  maze  of  distended  veins,  while  at  the  aortic  area  a  vibratory 
systolic  thrill,  pulsation,  and  a  variable  murmur  (systolic,  double, 
or  continuous)  may  develop.  Rupture  into  the  pulmonary  artery, 
which  is  unlikely  to  prove  so  rapidly  fatal  as  the  accident  just  men- 
tioned, causes  a  continuous  roaring,  vibratory  bruit,  accentuated 
during  systole,  most  intense  over  the  pulmonic  area,  and  occasionally 
accompanied  by  a  vibratory  thrill,  but  not  by  pulsation.  Preceding 
the  appearance  of  this  group  of  signs,  the  patient  is  suddenly  attacked 
by  an  alarming  paroxysm  of  dyspnea,  substernal  pain,  cough,  and 
hemoptysis,  symptomatic  of  the  actual  perforation. 

Aneurism  of  the  innominate  artery  produces  a  pulsatile  swelling 
at  the  right  sternoclavicular  articulation  or  in  the  suprasternal  notch, 
with  a  systolic  bruit  over  the  tumor  and  conducted  thence  into  the 
right,  but  not  into  the  left,  carotid.  There  may  be  duskiness  and 
puffiness  of  the  face,  indicating  pressure  upon  the  left  innominate  and 
deep  jugular  veins;  edema  of  the  right  arm,  due  to  obstruction  of 
the  right  subclavian  vein;  and  dyspnea  and  dysphagia,  in  conse- 
quence of  the  sac's  encroachment  upon,  and  lateral  dislocation 
of,  the  trachea  and  esophagus.  Violent  lancinating  pain  on  the  right 
side  of  the  head,  neck,  and  chest  and  down  the  right  arm  is  excited 
by  irritation  of  the  cervical  and  brachial  plexuses;  hiccough  and  res- 
piratory arhythmia  bespeak  compression  of  the  phrenic  nerve; 
and  pressure  symptoms  relating  to  the  pupils,  the  larynx,  and  the 
vasomotor  apparatus,  indicate  implication  of  the  sympathetic  and 
recurrent  laryngeal  nerves. 

If  the  common  carotid  artery  be  the  seat  of  a  circumscribed  aneurism, 
which  is  very  rarely  the  case,  the  dilatation  usually  occurs  on  the 
right  side  near  the  bifurcation  of  the  vessel,  at  the  level  of  the  thyroid 
cartilage,  where  a  pulsating  vascular  tumor  forms.  Should  the 
thoracic  portion  of  the  artery  be  implicated,  pressure  phenomena, 
similar  to  those  just  noted  and  corresponding  to  the  side  affected, 
sometimes  supervene,  and  if  there  be  pneumogastric  irritation,  vomit- 
ing, cardiac  disturbances,  and  respiratory  irregularities  are  to  be 
expected. 

Aneurism  of  the  stibcfawn  artery  most  commonly  is  situated  in 


DISEASES    OF   THE    CARDIOVASCULAR   SYSTEM  491 

the  third  division  of  this  vessel's  course  on  the  right  side,  and  shows 
as  a  pulsating  swelling  in  the  right  supraclavicular  fossa,  at  the 
subclavian  triangle.  Edema,  pain,  numbness,  and  loss  of  power  in 
the  corresponding  arm  may  occur  from  pressure  upon  the  subclavian 
vein  and  the  brachial  plexus;  hebetude,  vertigo,  disordered  vision, 
and  venous  engorgement,  from  interference  with  the  jugular  return 
flow;  and  respiratory  disturbances  and  hiccough,  from  irritation  of 
the  phrenic  nerve. 

The  systolic  thrill  and  murmur  of  aortic  atheroma,  with  the  asso- 
ciated arteriosclerosis,  suggest  aneurism  of  the  arch,  but  in  the 
former  condition  the  aortic  second  sound  is  high  pitched  and  ringing, 
and  there  is  no  abnormal  area  of  dulness,  no  systolic  pulsation,  and 
no  diastolic  shock.  The  differentiation  of  aortic  stenosis  and  aneu- 
rism is  considered  under  the  latter  lesion.  (See  p.  462.) 

Non-aneurismal  pulsations  in  the  suprasternal  notch  and  alongside 
the  manubrium,  due  to  cardiac  displacement,  enlargement,  and 
overaction,  are  to  be  distinguished  from  an  aneurismal  throb  in  this 
locality.  (See  Fig.  125,  p.  321.)  Dynamic  pulsation  of  the  aorta  may 
be  distinctly  felt  and  perhaps  seen  in  the  suprasternal  fossa,  and  may 
even  account  for  a  forcible  impact  beneath  the  upper  sternal  area. 
Pulsation  of  this  nature  is  commonly  met  with  in  neurotic,  anemic 
women  in  whom  no  other  signs  suggestive  of  aneurism  can  be  discov- 
ered, and,  moreover,  the  thoracic  pulsation  is  generally  synchronous 
with  violent  throbbing  of  the  abdominal  aorta.  Pulmonary  retraction, 
enlargement  of  the  right  heart,  cardiac  displacement,  and  dislocation 
of  the  aorta  by  a  crooked  spine  are  additional  causes  of  pulsation  in 
the  aortic  area,  but  in  such  instances  positive  evidence  of  aneurism 
is  lacking,  other  distinctive  physical  signs  are  demonstrable,  and  the 
previous  history  of  the  patient  furnishes  definite  information.  In 
general,  non-aneurismal  pulsations  are  strictly  systolic  and  more  or 
less  diffuse,  while  an  aneurismal  throb  is  distinctly  postsystolic,  and 
frequently  can  be  circumscribed  to  a  very  limited  area  of  the  chest- 
wall. 

Aneurism  may  be  suggested  by  acute  aortitis,  which  is  attended  by 
retrosternal  pain,  dyspnea,  precordial  oppression,  carotid  throbbing, 
pulse  irregularity,  and,  inconstantly,  parasternal  dulness  due  to  aortic 
dilatation.  In  aortitis,  however,  the  clinical  picture  develops  most 
abruptly;  bruit,  thrill,  and  diastolic  shock  are  lacking;  and  the  blood- 
pressure  of  the  two  radials  does  not  differ  conspicuously.  The  aor- 
titic  second  sound,  unlike  the  aneurismal,  may  have  a  peculiar  val- 
vular clanging  quality,  termed  by  Potain  the  bruit  de  tabourka,  from 
its  resemblance  to  the  sound  of  the  Oriental  native  drum  of  this 


492  PHYSICAL   DIAGNOSIS 

name.  Inasmuch  as  both  aortitis  and  aneurism  are  generally 
traceable  to  syphilis,  a  positive  Wassermann  test  is  not  distinctive, 
but  a  rontgenograph  may  prove  conclusive. 

Aortic  regurgitation  may  produce  pulsation  of  the  aorta,  and 
impaired  resonance  at  the  sternal  end  of  the  second  right  interspace, 
due  to  moderate  dilatation  of  the  ascending  arch.  But  in  pure 
Corrigan's  disease  all  the  accessible  arteries  are  found  to  beat  tumul- 
tuously,  an  ox-heart  is  datected,  a  water-hammer  pulse  is  common, 
and  a  characteristic  diastolic  bruit,  with  suppression  of  the  aortic 
second  sound,  is  audible.  Though  the  coexistence  of  aneurism  and 
aortic  regurgitation  may  be  suspected,  it  is  impossible  to  identify 
the  former,  save  by  the  #-rays,  unless  cardinal  signs  and  pressure 
symptoms  are  observed. 

Empyema  necessitates  resembles  aneurism  in  that  a  pulsating 
tumor  upon  the  chest-wall  is  common  to  both  conditions.  The  site 
of  an  empyematous  swelling  is  generally  below  and  outside  that  of 
an  aneurismal  tumor,  definite  signs  of  fluid  hi  the  left  pleura  are 
found,  thrill,  diastolic  shock,  and  expansile  pulsation  are  wanting, 
and  exploratory  puncture  shows  pus.  (See  Fig.  125,  p.  321.) 

Cervical  rib,  by  pressure  upon  the  subclavian  artery,  may  ac- 
count for  several  significant  aneurismal  signs  in  the  supraclavicular 
space — dull  pulsating  tumor,  thrill,  systolic  murmur,  and  difference 
in  the  radial  pulses,  but  in  an  instance  of  this  sort  the  x-ray  gives 
accurate  evidence  as  to  the  real  factor  of  the  puzzling  signs.  In 
some  cases  of  this  sort  the  anomalous  rib  hi  time  may  actually 
produce  fusiform  dilatation  of  the  blood-vessel. 

Pulmonary  tuberculosis  must  be  distinguished  from  so-called 
"aneurismal  phthisis,"  in  which  cough,  dyspnea,  hemoptysis,  foul 
sputum,  and  other  evidence  of  bronchial  catarrh,  bronchiectasis, 
and  pulmonary  infection  predominate.  Compression  of  a  bronchial 
tube  by  a  deep-seated  aneurism  springing  from  the  posterior  wall 
of  the  arch  may  account  for  such  a  symptom-group,  the  non-tuber- 
culous nature  of  which  is  to  be  inferred  if  the  sputum  be  habitually 
free  from  tubercle  bacilli,  if  the  ophthalmo-reaction  be  negative, 
and  if  there  be  no  wasting  or  other  constitutional  symptoms  of 
phthisis.  In  a  case  of  this  sort  radioscopy  may  effectually  settle 
the  diagnosis. 

Enlargement  of  the  thymus  gland  may  account  for  parasternal 
dulness  in  the  first  and  second  interspaces,  especially  on  the  left 
side,  but  dulness  from  this  cause,  unlike  that  of  an  aneurism, 
changes  to  resonance  when  the  subject,  heretofore  sitting  with 
the  chin  depressed,  retracts  the  head  to  the  fullest  extent,  thus 


DISEASES    OF    THE    CARDIOVASCULAR   SYSTEM  493 

forcing  the  pulmonary  margins  upward  over  the  gland  (T.  R. 
Boggs). 

The  differentiation  of  aneurism  from  mediastinal  neoplasm, 
adenitis,  and  abscess  is  considered  in  another  section.  (See  p.  307.) 

ANEURISM    OF    THE    ABDOMINAL    AORTA 

The  abdominal  aorta,  being  the  target  of  a  comparatively  feeble 
impact  by  the  blood  column,  is  less  commonly  the  seat  of  aneurism 
than  the  aortic  arch.  Although  sometimes  formed  by  the  posterior 
or  lateral  wall,  the  sac  usually  springs  from  the  anterior  aspect  of  the 
aorta  immediately  below  the  diaphragm,  in  the  region  of  the  celiac 
axis,  which  is  not  infrequently  also  implicated;  less  commonly  the 
dilatation  is  of  the  fusiform  variety.  The  aneurismal  tumor,  as  it 
enlarges,  encroaches  forward  into  the  epigastrium  and  the  left 
hypochondrium,  upward  beneath  the  diaphragm,  backward  against 
the  spine,  which  may  in  consequence  be  eroded,  and  perhaps  laterally 
as  far  even  as  the  left  flank.  Barring  those  extraordinarily  rare 
examples  of  spontaneous  clotting,  the  sac,  as  a  rule,  bursts  into  the 
retroperitoneum,  peritoneum,  pleura,  or  intestine,  while  an  arterio- 
venous  communication  with  the  inferior  vena  cava  is  a  possible  con- 
sequence. Some  patients  die  of  perforation  or  of  gangrene-peritonitis, 
secondary  to  embolism  of  the  superior  mesenteric  artery. 

The  physical  signs  of  an  accessible  aneurism  of  the  abdominal 
aorta  are  usually  clear  and  well  defined.  Inspection  shows  forcible 
systolic  pulsation  in  the  epigastric  area,  where  palpation  detects  a  dis- 
tinct tumor  having  a  typically  expansile  pulsation  and  systolic  thrill. 
On  percussion  it  is  sometimes  possible  to  distinguish  considerable 
impairment  of  abdominal  tympany  in  the  direction  of  the  left  epigas- 
trium, and  auscultation  affords  a  systolic,  if  not  a  double,  murmur 
over  the  site  of  the  swelling.  The  pulse  in  the  femoral  arteries  is 
likely  to  be  unnaturally  delayed  and  diminutive.  Important  pressure 
symptoms  may  arise,  affecting,  according  to  circumstances,  the  spine 
(vertebral  and  lumbar  pain,  paresthesia,  paralysis) ;  the  diaphragm 
(dyspnea) ;  the  vagus  (paroxysmal  vomiting) ;  the  inferior  vena  cava 
(edema  of  the  lower  extremities;  ascites) ;  the  esophagus  and  gut 
(dysphagia;  intestinal  obstruction);  and  the  ureters  and  common 
bile-duct  (renal  and  biliary  colic) . 

The  diagnosis  of  an  abdominal  aneurism  is  easily  made  when  an 
expansile  tumor  can  be  felt  beneath  the  belly-wall,  this  expanding 
property  of  the  pulsation  being  radically  different  from  the  lifting 
throb  of  a  normal  aorta  communicated  to  the  surface  by  an  over- 
lying mass  of  feces  or  by  an  abdominal  neoplasm;  moreover,  as 


494  PHYSICAL   DIAGNOSIS 

Osier  insists,  a  solid  tumor  (*.  e.,  of  the  pylorus,  pancreas,  or 
liver)  usually  falls  forward  away  from  the  aorta,  and  hence  ceases 
to  pulsate  when  the  patient  assumes  the  knee-chest  posture,  while 
an  aneurismal  pulsation  is  unaffected  by  this  maneuver.  The 
epigastric  throbbing  of  a  pulsating  ventral  aorta,  ordinarily  occurring 
in  neurotic,  anemic  females,  is  never  truly  expansile,  though  when 
pressed  upon,  the  vessel  may  generate  a  thrill  and  murmur. 


SECTION   VII 

EXAMINATION  OF  THE  ABDOMEN  AND  THE 
ABDOMINAL  VISCERA 


CLINICAL  ANATOMY 

UPON  the  surface  the  abdomen  extends  from  the  subcostal  angle 
and  costal  arch  to  the  pubic  crest  and  folds  of  the  groin,  being 
bounded  lateroposteriorly  by  the  iliac  crests,  flanks,  lower  ribs,  loins, 
and  vertebral  column.  Internally,  the  abdominal  cavity  reaches 
from  the  diaphragm  above  to  the  pelvic  outlet  below.  The  shape 
of  the  abdomen  varies  greatly  according  to  individual  differences 
determined  by  age,  sex,  muscular  development,  and  the  amount  of 
subcutaneous  and  omental  fat;  in  general,  it  conforms  to  the  out- 
line of  an  ovoid  bulged  centrally,  flattened  anteroposteriorly,  and 
longest  vertically.  Normally,  the  contour  should  follow  a  moderate 
convexity  the  gentle  curve  of  which  is  exaggerated  in  either  flank, 
and  shows  various  linear  depressions  and  local  elevations  correspond- 
ing to  the  anatomic  structures  of  the  parietes.  In  the  average  adult, 
however,  this  ideal  is  seldom  realized,  thanks  to  the  deforming  influ- 
ences of  corsets,  childbearing,  and  sedentary  habits.  In  a  man 
under  forty  years  of  age  the  abdominal  circumference  at  the  navel 
should  be  from  2  to  4  inches  (5  to  10  cm.)  less  than  the  thoracic 
circumference  at  the  nipple,  but  during  the  next  decade  these  two 
measurements  tend  to  become  equalized,  until,  at  fifty,  the  girth  of 
the  average  man's  belly  is  as  large  as,  if  not  larger  than,  that  of  his 
chest.  (Cf.  p.  70.)  In  a  woman  the  maximum  width  of  the  abdomen 
is  at  a  lower  level  than  in  a  man,  and  the  female  waist  line,  as  fixed  by 
dressmakers'  tradition,  should  be  about  10  inches  (25  cm.)  less  than 
the  bust  measurement.  In  a  child  the  greatest  abdominal  width  is 
in  the  upper  flanks,  and  the  belly,  as  a  whole,  is  relatively  large, 
owing  to  the  disproportionate  volume  of  the  liver  and  to  the  small 
size  of  the  pelvis,  whereby  the  intestines  and  bladder  are  crowded 
upward. 

As  anatomic  landmarks,  useful  in  the  physical  examination  of 

495 


496 


PHYSICAL    DIAGNOSIS 


the  abdomen,  there  is  available  a  number  of  parietal  markings  upon 
the  base  of  the  thorax  and  the  belly  musculature,  while,  in  suitable 
instances,  one  is  also  guided  by  certain  arbitrary  points  fixed  upon 
the  anterior  abdominal  wall  with  relation  to  underlying  viscera  (Fig. 
192;  cf.  Fig.  21).  The  upper  abdominal  region  presents  two  well- 
defined  surface  markings:  the  epigastric  hollow  of  the  scrobiculus 
cordis,  or  the  pit  of  the  stomach,  which  lies  directly  below  the  sub- 
costal angle  and  is  bounded  laterally  by  the  inner  borders  of  the 
seventh  costal  cartilages;  and  the  costal  arch,  diverging  on  either  side 


_  Scrobiculus  cordis  (in- 
frasternal  depression) 

Linea  alba  -J 
Tenth  costal  cartilage--,  PH^'Line*  transverse 

*    I  m-- 

Linea  semilunaris  I 

^^^^^^^^•^^^^^^K1  m  .7T~« 

Anterior  superior  iliac 

spine 

Symphysis  puhisB  — Poupart's  ligament 

Fig.  192- — Normal  abdominal  landmarks. 

from  the  apex  of  the  subcostal  angle  and  extending  thence  downward 
to  its  base  formed  by  the  tenth  costal  cartilage.  By  thrusting  the 
finger-tips  inward  between  this  point  and  the  iliac  crest  the  free 
extremities  of  the  eleventh  and  twelfth  ribs  can  be  palpated.  The 
important  bony  landmarks  of  the  lower  abdomen  are  the  pubic 
symphysis  and  the  anterior  superior  iliac  spines,  with  relation  to 
which  it  is  convenient  to  orient  lesions  of  the  lower  abdominal  zone. 
On  either  side  of  the  symphysis  lie  the  pubic  spines,  whence  the 
inguinal  ligaments  oj  Poupart  run  upward  to  the  anterior  superior 
spines  of  the  ilia.  The  most  conspicuous  anatomic  point  upon 


EXAMINATION  OF   ABDOMEN  AND  ABDOMINAL  VISCERA     497 

the  belly  wall  is  the  umbilicus,  or  navel,  which,  normally,  lies  in 
the  middle  line  at  about  the  level  of  the  highest  part  of  the  iliac  crests 
and  opposite  the  body  of  the  fourth  lumbar  vertebra.  Like  the 
nipple,  the  navel  has  a  most  variable  site:  it  is  considerably  lower  in 
children  than  in  adults,  and,  naturally,  shifts  its  position  when  the 
abdomen  is  overfat,  wasted,  distended,  or  pendulous  (v.  i.).  The 
linea  alba,  or  the  vertical  tendinous  white  line  between  the  recti 
muscles,  runs  from  the  tip  of  the  xiphoid  process  to  the  pubic  sym- 
physis,  and  can  usually  be  identified  as  a  narrow  median  furrow 
above  the  umbilicus,  below  which  point  its  course,  if  perceptible  at 
all,  is  indicated  by  a  linear  deposition  of  pigment  (linea  nigra) ,  or,  in 
men,  by  a  matted  line  of  converging  hairs.  In  a  well-muscled  man 
two  or  three  linea  transverse  of  the  rectus  abdominis  are  visible 
as  horizontal  furrows,  at  the  level  of  the  seventh  costal  cartilage, 
at  the  base  of  the  costal  arch,  and  just  below  the  umbilicus. 
The  linea  semilunares,  corresponding  to  the  outer  borders  of  the 
recti,  extend  downward,  with  a  moderate  outward  curve,  from  the 
ninth  costal  cartilage  to  a  point  midway  between  the  umbilicus  and 
the  anterior  superior  iliac  spine,  and  thence  to  the  pubic  spine.  In 
the  obese  abdomen  horizontal  cutaneous  flexion-folds  are  frequently 
visible,  one  at  the  level  of  the  umbilicus  and  another  about  an  inch 
(2.5  cm.)  above  the  pubes.  The  lateral  walls  of  the  abdomen 
between  the  thorax  and  the  ileum  form  the  flanks,  which,  lacking 
rigid  osseous  and  muscular  support,  commonly  form  a  moderate 
local  bulging  below  the  costal  arch.  Posteriorly,  the  abdomen  is 
supported  by  the  pelvic  walls,  the  lower  ribs,  and  the  spinal  column, 
whose  median  furrow  extends  downward  to  the  sacral  triangle  or  the 
shallow  depression  overlying  the  sacrum.  The  region  of  the  loin 
includes  that  part  of  the  back  between  the  twelfth  rib  and  the  iliac 
crest. 

The  course  of  the  abdominal  aorta  is  indicated  by  a  line  directly 
to  the  left  of  the  linea  alba  drawn  from  the  ensiform  to  the  level  of 
the  highest  part  of  the  iliac  crest.  At  this  level  (f  inch,  or  19  mm. 
below  the  navel)  the  aorta  divides  into  the  two  common  iliac  arteries 
which  diverge  toward  a  point  midway  between  the  anterior  superior 
iliac  spine  and  the  pubic  symphysis.  The  celiac  axis  corresponds 
to  a  point  on  the  aortic  line  about  4  or  5  inches  (10  or  12.5  cm.) 
above  the  navel,  and  between  these  two  levels,  from  above  down- 
ward, lie  the  superior  mesenteric  artery,  the  renal  arteries,  and  the 
injerior  mesenteric  artery.  The  deep  epigastric  artery  follows  a  line 
extending  from  the  umbilicus  to  the  middle  of  Poupart's  ligament. 
The  inferior  vena  cava,  lying  to  the  right  of  the  aorta,  virtually 
32 


498 


PHYSICAL   DIAGNOSIS 


follows  the  surface  markings  of  this  vessel,  its  left  common  iliac 
branch  being  crossed  by  the  right  common  iliac  artery  just  below 
the  aortic  bifurcation. 


TOPOGRAPHIC  LINES  AND  AREAS 

As  an  aid  in  determining  the  exact  position  of  the  abdominal 
organs  and  the  lesions  thereof  the  surface  of  the  abdomen  may  be 
divided  by  two  vertical  and  two  horizontal  lines  into  seven  definite 
areas1  (Fig.  193)  The  two  vertical  or  Poupart's  lines  are  indicated 


Poupart's  vertical  -f 


Infracostal 


Intcrspinal 


Fig.  193. — Topographic  lines  of  the  abdomen. 

by  the  downward  continuation  of  the  right  and  left  midclavicu- 
iar  lines,  and  extend  perpendicularly  from  the  tip  of  the  ninth  costal 
cartilage  to  a  point  on  Poupart's  ligament  midway  between  the 
anterior  superior  iliac  spine  and  the  pubic  symphysis.  Of  the  two 
horizontal  lines,  the  upper  one,  or  the  infracostal,  joins  the  lower 
borders  of  the  tenth  costal  cartilages  and  passes  backward  to  meet 
the  line  of  the  twelfth  thoracic  vertebra  at  the  posterior  axillary 
line.  The  lower  horizontal  line,  or  the  interspinal,  connects  the  two 

1  The  two  abdominothoracic  regions  (hypochondriac  or  inframammary)  are 
described  in  connection  with  Topographic  Areas  of  the  Thorax,  on  page  77. 


EXAMINATION   OF  ABDOMEN  AND   ABDOMINAL  VISCERA     499 


anterior  superior  iliac  spines  and  runs  posteriorly  to  the  vertebral 
column  along  the  iliac  crests.     (See  p.  77.) 

The  topographic  areas  (Fig.  194),  delimited  by  the  foregoing  lines, 
are  designated,  from  above  downward,  on  the  anterolateral  aspects 
of  the  belly  as  follows: 

The  epigastric  region,  lying  between  the  borders  of  the  costal 
arch  and  the  infracostal  line,  overlies  the  liver,  gall-bladder,  stomach, 
duodenum,  pancreas,  and  kid- 
neys. 

The  umbilical  region,  or 
the  central  rectangular  area 
formed  by  the  crossing  of  the 
horizontal  and  the  vertical 
lines  on  the  anterior  abdom- 
inal wall.  Beneath  this  sur- 
face area  lie  the  transverse 
colon,  small  intestine,  mesen- 
tery, greater  omentum,  and 
kidneys. 

The  hypogastric  or  pubic 
region,  extending  from  the 
interspinal  line  to  the  pubic 
bone  and  bounded  laterally 
by  Poupart's  lines.  The 
hypogastrium  corresponds  to 
the  coils  of  the  ileum,  the 
sigmoid  flexure,  the  cecum 
(and  frequently  the  appen- 
dix), the  gravid  uterus,  and 
the  normal  bladder  in  the 
child,  or  the  distended  blad- 
der in  the  adult. 

The  lumbar  region,  on  either  side  of  the  umbilical  area  and 
between  the  infracostal  and  interspinal  lines,  the  posterior  con- 
tinuations of  which  it  lies  between  from  Poupart's  line  to  the 
spinal  column.  In  the  right  lumbar  region  are  the  ascending 
colon,  ileum,  and  right  kidney,  and  in  the  left,  the  descending 
colon,  jejunum,  and  left  kidney. 

The  iliac  or  inguinal  region,  consisting  of  a  triangular  area  in  each 
groin  bounded  by  Poupart's  ligament,  Poupart's  line,  and  the  inter- 
spinal line.  The  cecum,  vermiform  appendix,  and  ileum  occupy 
this  region  on  the  right  side,  and  the  sigmoid  colon,  ileum,  and  jeju- 
num, on  the  left. 


Fie 


14. — Topographic  regions  of   the  ab- 
domen. 


$00  PHYSICAL   DIAGNOSIS 

METHODS  OF  ABDOMINAL  EXAMINATION 

All  four  of  the  cardinal  methods  of  physical  diagnosis  are  applicable 
to  the  examination  of  the  abdomen,  according  to  the  exigencies  of 
the  individual  case,  but  in  routine  work  inspection  and  palpation 
are  chiefly  relied  upon,  percussion  being  mainly  a  confirmatory 
step,  and  auscultation  being  resorted  to  only  in  exceptional  instances. 
Mensuration  is  commonly  used  in  connection  with  these  procedures, 
to  fix  the  exact  position  of  pathologic  signs,  and  to  ascertain 
abdominal  circumferences  and  surface  distances.  As  already  pointed 
out,  the  aspirating  needle  is  sometimes  indispensable  in  dealing  with 
abdominal  lesions,  and  occasionally  this  is  also  true  of  the  #-ray. 

The  general  principles  of  the  preceding  steps  will  be  outlined 
below,  and  their  special  application  under  both  normal  and  pathologic 
circumstances  considered  in  connection  with  the  examination  of 
the  different  abdominal  organs.  (See  p.  519  et  seq.) 

For  a  general  examination  of  the  abdomen,  which  should  be  bare 
from  epigastrium  to  pubes,  the  dorsal  decubitus  is  ordinarily  chosen, 
the  subject  lying  upon  the  back  in  an  unconstrained,  symmetric 
posture,  with  the  knees  drawn  up  and  the  shoulders  elevated  by  a 
pillow,  and  breathing  deeply  with  the  mouth  wide  open.  Attention 
to  these  details  favors  relaxation  of  the  musculature,  so  essential  for 
dependable  results  from  visual  and  tactile  examination.  Stubborn 
rigidity  of  the  belly  wall,  the  bane  of  successful  palpation,  may  have 
to  be  overcome  by  anesthesia  or  by  the  somewhat  impracticable, 
though  efficacious,  expedient  of  immersing  the  patient  in  a  warm 
bath.  Small  talk,  to  divert  the  patient's  attention,  will,  however, 
generally  induce  sufficient  muscular  relaxation  to  allow  a  satisfactory 
examination. 

The  erect  position  is  indicated  in  the  investigation  of  certain  types 
of  abdominal  enlargement  and  anomalies  of  contour,  due,  for  example, 
to  visceral  prolapse,  to  tumor,  or  to  sagging  of  the  parietes.  Lateral 
decubitus  upon  the  unaffected  side  is  useful  in  searching  for  unilateral 
enlargements,  as  of  the  liver  and  the  spleen,  and  in  comparing 
the  postural  changes  of  the  percussion  sound  elicited  with  the 
patient  in  dorsal  recumbency,  as  in  intra-abdominal  accumulations 
of  fluid.  The  knee-chest  posture  is  employed  when  attempting  to 
palpate  small  abdominal  masses  and  in  testing  the  effect  of  gravity 
upon  a  pulsating  tumor,  which,  if  aneurismal,  continues  to  heave 
despite  the  subject's  genupectoral  attitude,  whereas,  if  the  pulsation 
be  transmitted  from  the  aorta  to  an  overlying  tumor,  it  ceases  when 
the  pressure  upon  the  vessel  is  relieved  by  this  maneuver. 

Inspection  shows  the  size  and  configuration  of  the  abdomen,  the 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     501 

condition  of  the  skin  and  subcutaneous  structures,  and  the  character 
of  various  movements  visible  upon  the  surface.  By  this  method  of 
inquiry,  then,  the  following  details  are  investigated:  deviations  from 
the  normal  contour  of  the  belly  relating  to  its  general  enlargement  or 
retraction  and  to  local  prominences;  the  color  and  nutrition  of  the 
skin  and  the  presence  or  absence  of  edema,  eruptions,  scars,  dilated 
veins,  enlarged  glands,  and  other  subcutaneous  nodules;  and  the 
movements  of  the  parietes  due  to  respiration,  peristalsis,  and  cardio- 
vascular pulsation.  Perfect  symmetry  of  posture  is  necessary,  in  order 
to  recognize  slight  deviations  from  the  normal  contour  of  the  abdo- 
men, which  should  be  inspected  from  several  viewpoints — anterior, 
oblique,  and  lateroposterior — according  to  the  requirements  of  the 
examination.  The  light  should  fall  obliquely,  not  perpendicularly, 
upon  the  surface,  so  as  to  exaggerate  trifling  peculiarities  of  form 
and  of  movement. 

Palpation  not  only  confirms  many  of  the  signs  obtained  visually, 
but  also  is  the  means  of  investigating  the  sensitiveness  of  a  part 
and  the  tension  of  the  abdominal  wall;  of  detecting  tumors  and  fixing 
their  site,  mobility,  and  consistence;  and  of  recognizing  fluctuation, 
pulsation,  thrills,  and  friction-rubs.  An  educated  sense  of  touch  is 
as  important  in  studying  abdominal  lesions  as  is  a  trained  ear  in 
interpreting  cardiac  and  pulmonary  sounds.  Muscular  relaxation 
having  been  secured,  the  palpating  hand  is  gently  laid,  palm  down- 
ward, upon  the  surface  of  the  abdomen,  and,  with  firm  but  gentle 
pressure,  the  general  contour  of  the  underlying  structures  is  deter- 
mined. Taking  advantage  of  the  phases  of  expiration,  when  the 
abdominal  wall  is  relaxed,  a  deep  and  sliding  method  of  palpa- 
tion, from  right  to  left  and  from  above  downward,  frequently 
enables  one  to  outline  with  fair  accuracy  the  stomach  and  the 
large  intestine,  if  undue  force  is  not  used.  Should  a  point  of 
resistance  be  found,  its  shape,  motility,  and  density  are  ascer- 
tained by  deeper  pressure  with  the  fingers,  still  keeping  the  palm 
of  the  hand  close  to  the  surface  and  avoiding  abrupt  pressure  with 
the  finger-tips.  This  only  tickles  the  patient  and  excites  a  local 
spasm  of  board-like  rigidity.  It  may  be  added  that  a  cold  hand 
placed  upon  the  belly  will  chill  it  into  a  similar  contraction.  The 
entire  surface  of  the  abdomen  is  covered  in  the  manner  described, 
the  hand  traveling  consecutively  over  the  different  areas,  the  con- 
tents of  which  are  meanwhile  rehearsed  by  the  examiner.  Nervous- 
ness of  the  patient,  abdominal  tenderness,  and  fat,  muscular,  or 
edematous  parietes  are  the  principal  difficulties  that  interfere  with 
one's  tactile  appreciation.  When  the  organs  are  not  palpable  because 
of  ascites,  it  is  well  to  try  "dipping,"  which  consists  of  a  series  of 


502  PHYSICAL   DIAGNOSIS 

sudden  deep  downward  thrusts  with  the  finger-tips  over  the  enlarge- 
ment sought  for.  This  manipulation  momentarily  displaces  the  fluid 
overlying  the  obscure  viscus  or  tumor  so  that  it  may  be  felt  plainly. 

Bimanual  palpation  of  the  abdomen  is  performed  with  the  patient 
in  dorsal  decubitus,  the  examiner  being  seated  by  the  bedside  and 
palpating  the  anterolateral  surface  of  the  belly  with  one  hand,  while, 
with  the  other  hand  applied  posteriorly,  firm  upward  pressure  is 
made  against  the  relaxed  structures  of  the  loin  and  flank  of  the 
corresponding  side.  This  procedure,  aside  from  facilitating  the 
palpation  of  fixed  viscera  like  the  liver  and  the  spleen,  is  also  useful 
in  the  tactile  examination  of  movable  solid  bodies  within  the  abdomi- 
nal cavity — tumors,  enlarged  glands,  and  movable  kidneys.  In  out- 
lining solid  intra-abdominal  masses  H.  A.  Kelly  practises  "  bimanual 
vibratory  palpation,"  which  consists  of  making  a  succession  of  rapid 
tremulous  movements  with  the  palpating  fingers  over  the  surface  of 
the  mass,  whereby  these  tactile  impressions  are  conducted  to  the 
underlying  hand. 

Mensuration  is  a  valuable  adjunct  to  the  foregoing  methods,  in 
that  comparative  measurements  of  the  abdominal  circumference  and 
of  various  surface  distances  indicate  the  progressive  changes  in  the 
size  of  the  belly  that  attended,  for  example,  ascites,  leukemic  spleno- 
megaly, and  large  neoplasms.  The  abdominal  girth  is  usually  meas- 
ured at  the  level  of  the  umbilicus,  and  from  this  point  it  is  also  con- 
venient to  compute  mural  distances,  upward  to  the  tip  of  the  xiphoid, 
downward  to  the  pubic  symphysis,  and  obliquely  to  the  anterior 
superior  iliac  spines. 

Percussion  of  the  abdomen  is  resorted  to  principally  as  a  means 
of  confirming  the  data  obtained  by  inspection  and  palpation,  in  com- 
parison with  which  percussion,  as  an  individual  method  of  inquiry, 
is  of  distinctly  inferior  value.  According  to  the  technic  and  principles 
elsewhere  described  (p.  12  et  seq.),  abdominal  percussion  is  employed 
chiefly  in  delimiting  the  boundaries  of  the  liver  and  the  spleen,  in 
detecting  overdistention  of  the  bladder,  and  in  corroborating  the 
visual  evidences  of  meteorism  and  of  fluid  within  the  peritoneal 
cavity.  Forced  inspiration  on  the  part  of  the  patient,  which  de- 
presses the  viscera  and  approximates  them  to  the  abdominal  wall, 
aids  the  judgment  of  percussion  signs. 

The  normal  tympany  of  the  abdomen  varies  in  intensity,  pitch, 
and  duration  with  the  volume  and  pressure  of  air  in  the  viscus  per- 
cussed. If  no  disproportionate  distention  exists,  the  stomach 
emits  louder,  lower-pitched,  and  better  sustained  tympany  than  the 
intestines,  and  the  same  is  true  of  the  tympany  afforded  by  the  large 
gut  ia  comparison  with  that  of  the  small.  Abdominal  tympany  is 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     503 

exaggerated  by  meteorism,  and  variously  impaired  by  factors  such 
as  emptiness  and  collapse  of  the  bowels  or  by  fecal  masses  therein, 
distention  of  the  urinary  bladder,  fluid  effusions,  neoplasms,  and 
enlargements  of  the  various  abdominal  organs.  Auscultatory  per- 
cussion affords,  in  skilled  hands,  an  accurate  method  of  outlining  the 
stomach,  of  discovering  abnormalities  in  the  size  and  position  of 
the  gut,  and  of  localizing  intra-abdominal  tumors. 

Auscultation  is  generally  dispensed  with  in  a  routine  examination 
of  the  abdomen,  since  its  usefulness  is  limited  to  special  conditions. 
The  sounds  audible  over  the  abdomen  are  chiefly  intestinal  and  gastric, 
less  commonly  frictional,  and  rarely  of  cardiovascular  origin.  The 
normal  intestines  are  the  seat  of  a  medley  of  liquid  gurgles  and 
sonorous  and  sibilant  cooing  sounds  caused  by  the  rush  of  gas 
through  the  unequal  lumen  of  the  gut.  Should  the  latter  be 
stenosed  such  sounds  are  greatly  intensified,  provided  that  intestinal 
peristalsis  persists.  Over  the  stomach  the  transmitted  heart  and 
voice  sounds  are  sometimes  heard  as  hollow  metallic  echoes,  and 
here  also  the  bubbling  and  splashing  of  fluid  within  the  stomach 
may  be  detected.  In  gastric  dilatation  and  in  fermentive  gastritis 
these  noises  are  exaggerated  and  intermingled  with  a  curious  sort  of 
seething  effervescence.  The  various  kinds  of  friction  are  more  often 
to  be  recognized  by  auscultation  than  by  tactile  sense.  Peritoneal 
friction,  which  does  not  differ  acoustically  from  the  pleural  rub,  is 
generally  excited  only  by  respiration,  although,  rarely,  active  peristal- 
sis of  the  gut  is  the  exciting  factor  of  the  sound.  The  sounds  of 
tubercle  friction  and  of  gall-stone  crepitus  possess  a  harsh  crunching 
quality  and  are  best  elicited  by  combined  auscultation  and  pal- 
pation. In  infants  and  young  children  the  respiratory  sounds,  as 
well  as  pulmonary  and  pleural  adventitious  sounds,  are  distinctly 
audible  over  the  abdomen  (H.  L.  K.  Shaw).  The  abdominal  aus- 
cultatory  signs  of  cardiovascular  origin  include  the  fetal  heart  sounds 
and  the  uterine  souffle  of  pregnancy;  the  murmurs  of  hepatic  cir- 
rhosis and  of  splenomegaly;  the  bruits  of  aneurism  and  of  compres- 
sion of  the  abdominal  aorta;  and  the  hollow  echo  of  a  heart  murmur 
transmitted  downward  and  amplified  by  an  air-filled  viscus  and  by 
the  telephonic  properties  of  the  parietes. 

CLINICAL  TYPES  OF  ABDOMEN 

Several  intra-abdominal  affections  account  for  conspicuous 
deviations  from  the  normal  size  and  shape  of  the  abdomen,  as  in 
ascites,  visceral  ptosis,  intestinal  or  peritoneal  meteorism,  and  states 
of  extreme  inanition,  in  all  of  which  the  abnormal  configu- 


5°4 


PHYSICAL    DIAGNOSIS 


ration  of  the  belly  may  present  a  most  distinctive  clinical  picture. 
Abdominal  enlargements  belonging  to  this  group  are  to  be  distin- 
guished from  those  symptomatic  of  obesity  and  of  pregnancy,  which, 
for  the  sake  of  comparison,  will  be  considered  in  connection  with 
these  pathologic  types. 

The  Obese  Abdomen. — In  abdominal  enlargement  due  to  this 
very  common  cause  the  subcutaneous  deposition  of  fat  can  be  easily 
identified  by  rolling  a  fold  of  the  skin  between  the  fingers.  Ordinarily 

the  belly  protrudes  as  a  sym- 
metric globular  enlargement 
which  depresses  the  navel,  ac- 
centuates the  cutaneous  flex- 
ion-folds, arches  the  pit  of  the 
stomach,  and  encroaches  upon 
the  flanks  and  the  pubes;  or, 
should  the  musculature  be 
relaxed  and  flabby,  the  ab- 
domen may  be  pendulous, 
creased  by  deep  transverse 
furrows,  and  lobulated  by  ir- 
regular islands  of  fat  (Fig. 

I95)- 
The   Scaphoid  Abdomen. 

— The  scaphoid  abdomen,  or 
boat-shaped  belly,  typifies  the 
extreme  stage  of  abdominal 
retraction  and  wasting  conse- 
quent to  intestinal  emptiness 
and  contraction,  to  disappear- 
ance of  the  panniculus  adi- 
posus,  and  to  tonic  spasm  of 
the  parietal  musculature.  In 
the  typical  instance  the  ab- 
domen is  sunken  or  hollowed 
out  like  a  basin  or  a  boat,  whose  sides  closely  correspond 
to  the  concavity  of  the  bony  pelvis.  The  flanks  are  deeply 
indented,  the  costal  margins  converge  and  thus  narrow  the  sub- 
costal angle,  the  xiphoid  and  Poupart's  ligaments  stand  out  con- 
spicously,  and  the  iliac  crests  rise  high  above  the  surface  of  the 
sunken  belly.  The  abdominal  viscera  and  other  structures  are 
palpable  as  distinctly  as  if  the  subject  were  an  anatomic  model, 
and  the  area  of  normal  abdominal  tympany  is  greatly  restricted, 
while  pulmonary  resonance  usually  extends  below  its  normal  limit. 


Fig. 195. — The  obese,  relaxed  abdomen  (Jef- 
ferson Hospital). 


EXAMINATION   OF   ABDOMEN   AND   ABDOMINAL    VISCERA     50$ 

Extraordinary  bodily  wasting  commonly  attends  these  abdominal 
changes,  and  to  such  extremes  may  the -general  emaciation  progress 


Fig.  196. — The  scaphoid  abdomen  (Philadelphia  General  Hospital). 

that  the  patient,  as  the  accompanying  picture  testifies,  literally  may 
become  a  living  skeleton  (Fig.  196).     The  scaphoid  abdomen  is  met 
with  in  its  typical  form  in  tuberculous  meningitis,  in  chronic  perito- 
nitis, and  in  states  of  inanition  inci- 
dent to   prolonged   vomiting,    chronic 
diarrhea,  and  stricture  of  the  gullet  or 
the  pylorus.     It  has  been  observed  also 
in  simple  meningitis,  in  cerebral  tumor, 
and  in  the  colic  of  plumbism. 

The  Abdomen  of  Pregnancy. — 
Flattening  of  the  hypogastrium,  appre- 
ciable by  or  before  the  third  month 
after  conception,  is  the  earliest  visible 
change  in  the  abdominal  contour  caused 
by  a  gravid  uterus.  By  the  fourth 
month  this  gives  way  to  suprapubic 
fulness,  which  progressively  increases 
and  extends  upward  at  the  rate  of 
about  |  inch  (1.9  cm.)  each  fortnight, 
until  by  the  sixth  month  the  swelling 
reaches  the  level  of  the  umbilicus,  and 
by  the  eighth  month,  the  xiphoid. 
During  the  later  months  of  gestation 
the  abdomen  presents  a  general  enlarge- 
ment, which,  from  an  anterior  aspect, 
with  the  subject  erect,  is  of  roughly  pyriform  shape,  with  the  tapered 
end  below,  while  the  profile  of  the  belly  shows  a  symmetric  protu- 
berance more  marked  anteroposteriorly  than  laterally  (Fig.  197). 
Primarily,  the  enlargement  extends  upward  in  the  median  line,  but 
later  a  slight  dextral  deflection  is  commonly  noted,  and  the  shape  is 
but  slightly  altered  by  postural  changes.  The  flanks  are  uniformly 


Fig.  197. — The  abdomen  of  preg- 
nancy (Jefferson  Hospital). 


506 


PHYSICAL   DIAGNOSIS 


rounded,  the  subcostal  angle  is  moderately  widened,  and  the  navel, 
at  first  depressed,  gradually  rises  to  the  surface,  and  finally  pouts 
prominently.  These  changes,  observed  in  primiparse  with  firm 
abdominal  walls,  are  naturally  subject  to  modifications  of  contour 
in  women  whose  parietes  have  been  unduly  stretched  by  previous 
childbirth  or  by  visceral  ptosis,  under  which  circumstances  anterior 
bulging  and  sagging  of  the  dependent  part  of  the  abdomen  are 
especially  conspicuous.  Of  the  numerous  associated  objective 
evidences  of  pregnancy,  those  of  special  interest  to  the  clinician  include 
the  fetal  cardiac  sounds,  the  uterine  bruit,  abdominal  ballottement, 
a  palpable  fetal  outline,  mammary  changes, 
striae  gravidarum,  and  overfulness  of  the 
superficial  veins. 

The  Ascitic  Abdomen. — Alterations  in 
the  appearance  of  the  abdomen  due  to 
ascites,  or  dropsy  of  the  peritoneal  cavity, 
vary  with  the  volume  of  the  contained  fluid 
and  the  pressure  thereby  produced.  If  the 
effusion  be  moderate,  nothing  more  definite 
is  perceptible  than  slight  bulging  of  the 
flanks  with  flattening  of  the  belly's  summit, 
in  the  dorsal  posture,  with  unnatural  ful- 
ness of  the  lower  abdomen  when  the  patient 
stands  erect.  The  dependent  parts  afford 
a  dull  or  a  flat  percussion  sound  which 
shifts  with  change  of  posture  and  conse- 
quent gravitation  of  the  fluid  and  ascent 
of  the  buoyant  intestines.  With  the  sub- 
ject in  dorsal  decubitus,  the  flanks  are  flat 
(fluid)  and  the  summit  of  the  abdomen  is 
tympanitic  (gut),  but  when  the  patient  turns 
upon  the  side  the  opposite  flank,  origin- 
ally flat,  will  become  tympanitic  as  the  intestines  float  upward  upon 
the  surface  of  the  gravitated  fluid  and  lie  directly  beneath  the  pari- 
etes under  the  examiner's  pleximeter  finger.  In  the  knee-chest 
posture  both  flanks  give  tympany,  while  the  central  part  of  the 
abdomen  is  flat.  These  percussion  changes,  it  must  be  understood, 
may  not  be  perceptible  in  a  small  effusion  (of  less  than  50  ounces, 
or  1500  cc.),  nor  when  it  is  so  large  as  to  prevent  contact  between 
the  gut  and  the  parietes. 

If  the  effusion  be  of  large  volume  there  is  a  proportionately  strik- 
ing enlargement  of  the  abdomen,  in  the  form  of  a  smooth,  tense,  uni- 
form globular  protuberance  which  curves  downward  from  the 


Fig.  19*5. — The  ascitic  abdo- 
men (Jefferson  Hospital). 


EXAMINATION   OF    ABDOMEN   AND   ABDOMINAL    VISCERA     507 

epigastrium,  fills  the  flanks,  overhangs  the  hypogastrium,  and  oblit- 
erates the  umbilical  fossa,  if,  indeed,  the  navel  does  not  actually 
protrude  from  the  surface  (Fig.  198).  The  shape  of  the  abdomen 
distended  to  such  a  degree  is  slightly,  if  at  all,  affected  by  postural 
changes,  and,  provided  that  the  mural  tension  be  not  excessive,  the 
fluid  will  give  a  distinctive  wave  of  fluctuation,  recognizable  commonly 
by  the  eye  as  well  as  by  the  palpating  hand.  (See  p.  516.)  A 
pendulous  abdomen  full  of  free  fluid  bulges  particularly  toward  the 
middle  line,  so  as  to  produce  a  disproportionately  elongated  protu- 
berance having  a  broad,  sagging  base,  the  shape  of  which  visibly  alters 
when  the  subject  changes  from  the  erect  to  the  recumbent  position. 
The  abdominal  cavity  alone  may  be  dropsical,  as  is  generally  the 
case  in  hepatic  cirrhosis,  in  tuberculous  peritonitis,  and  in  Pick's  dis- 
ease; or  the  ascites  may  be  part  and 
parcel  of  an  anasarca  of  cardiorenal 
origin,  in  which  event  the  edema  also 
invades  the  abdominal  wall  to  a  greater 
or  less  extent. 

The  Gaseous  Abdomen. — The  dis- 
tention  symptomatic  of  tympanites  or 
meteorism  may  be  most  extraordinary, 
the  abdomen  becoming  symmetrically 
ballooned  in  the  form  of  a  tense  tym- 
panitic  sphere  which  preserves  the  same 
contour  irrespective  of  postural  change, 
and  whose  pressure  upon  the  dia- 
phragm embarrasses  the  respiratory 
movements  and  disorders  the  cardiac 
action  (Fig.  199;  cf.  Fig.  211).  A  veri- 
table "  wind  bomb  "  in  the  belly  is  the 
apt  description  of  this  condition  found 
in  one  of  Ben  Tonson's  plays.  The 

.    .        .      ,          ,,  .11  Fig.  199. — The  gaseous  abdomen 

abdominal  walls  are  universally  taut,  (Jefferson  Hospital), 

smooth,  and  shiny,  the  umbilicus  is  on 

a  level  with  the  surface  or  protrudes  above  it,  and  in  the  extreme 
case  the  lower  part  of  the  bony  thorax  projects  anterolaterally. 
In  gastro-intestinal  meteorism  it  is  sometimes  possible  to  distin- 
guish the  contour  and  the  peristaltic  movements  of  the  gaseous 
stomach  and  gut,  but  in  meteorism  due  to  the  accumulation  of  gas 
within  the  peritoneal  cavity  the  abdomen  is  uniformly  enlarged  and 
neither  the  outline  of  the  gastro-intestinal  tube  nor  any  movement 
thereof  is  perceptible.  (See  p.  533.)  The  tympany  of  intestinal 
meteorism  encroaches  upon,  displaces,  and  perhaps  obliterates  the 


508 


PHYSICAL   DIAGNOSIS 


areas  of  hepatic  and  splenic  flatness.  In  pneumoperitoneum  the 
property  of  the  intraperitoneal  free  gas  to  seek  the  highest  level 
may  afford  a  most  distinctive  alteration  of  the  percussion  sound 
when  the  patient  turns  from  dorsal  to  left  lateral  decubitus.  In 
the  dorsal  posture,  despite  the  replacement  of  hepatic  flatness  by 
tympany  anteriorly,  dulness  persists  laterally  in  the  right  axillary 
region,  but  if  the  subject  turns  upon  the  left  side  this  axillary  dul- 
ness at  once  changes  to  tympany,  inasmuch  as  the  free  gas  rises  to 
fill  the  space  beneath  the  parietes  created  by  the  gravitation  of  the 
liver  toward  the  dependent  side. 

Unfortunately,  this  changeable  dulness  in  the  axilla  is  not  always 
demonstrable,  for  hepatic  dulness  may  be  wholly  obliterated  by  a 
^  ,  greatly  distended  colon.  In  such  in- 

stances, then,  the  only  certain  means 
of  differentiating  pneumoperitoneum 
and  intestinal  meteorism  is  an  ex- 
ploratory puncture  of  the  peritoneal 
cavity.  (See  p.  56.) 

The  Gastroptotic  Abdomen.  — 
When  the  subject  stands  erect,  gas- 
troptosis,  or  downward  displacement 
of  the  stomach,  produces  a  bulging 
that  appears  most  conspicuous  in  the 
umbilical  region,  with  deepening  of  the 
epigastrium,  leveling  of  the  umbilical 
depression,  and  a  variable  degree  of 
flaccidity  and  thinning  of  the  parietes 
(Fig.  200).  In  typical  examples  the 
abdominal  contour  is  a  fairly  sym- 
metric curve  from  the  infracostal 
line  to  the  pubes,  the  flanks  are  flat 
or  even  hollow,  and  each  groin  is 
seamed  by  a  deep  furrow  paralleled 
above  by  a  local  saugage-shaped  bulg- 
ing of  the  belly  wall.  When  gastrec- 

tasis,  or  dilatation  of  the  stomach,  coexists,  as  it  usually  does,  the 
epigastric  hollow  is  generally  effaced  rather  than  deepened,  and 
unnatural  fulness  at  the  inner  borders  of  the  lumbar  regions  is  also 
noticeable. 

The  Enteroptotic  Abdomen. — Enteroptosis,  or  downward 
displacement  of  the  intestines,  is  almost  invariably  associated  with 
descent  of  the  stomach  and  of  other  abdominal  viscera,  of  which  acci- 
dents, generically  designated  as  Gltnard's  disease,  relaxation  of  the 


Fig.  200. — The   gastroptotic  ab- 
domen (Jefferson  Hospital). 


EXAMINATION  OF   ABDOMEN  AND   ABDOMINAL  VISCERA     509 


mesentery,  peritoneum,  and  parietes  is  the  exciting  cause  (Fig.  201). 
In  the  upright  posture  enteroptosis  produces  a  most  characteristic 
alteration  in  the  size  and  shape  of  the  abdomen,  whose  enlarged 
profile  may  be  likened  to  that  of  a  gourd  or  of  a  sagging  sac,  while 
the  anterior  aspect  is  roughly  pear  shaped,  with  an  evenly  rounded 
base.  The  anterior  abdominal  wall  slopes  gently  downward  from 
the  epigastrium  to  the  navel,  where  it  bulges  in  all  directions  into  a 
huge  flabby  paunch,  full  of  distended  and  constipated  gut,  hanging 
far  beyond  and  below  the  pubes,  and 
overlapping  laterally  to  form  deep 
cutaneous  folds,  often  painfully  ex- 
coriated, which  course  obliquely  up- 
ward as  far  as  the  summits  of  the  iliac 
crests.  There  is  unnatural  flattening 
of  the  epigastric  concavity  and  more 
or  less  effacement  of  the  umbilical  de- 
pression, and  the  abdominal  wall  is 
generally  wasted,  stretched,  and  dis- 
figured by  silvery  striations.  With 
the  subject  in  dorsal  decubitus,  the  out- 
lines of  the  stomach  and  intestines  may 
be  distinctly  visible,  owing  to  the  pa- 
rietal thinning  and  relaxation,  and  in 
the  extreme  instance,  there  may  be 
a  hernial  protrusion  of  the  abdominal 
viscera  through  a  separation  between 
the  recti  abdominales.  When  enterop- 
tosis and  obesity  are  combined  a  most 
peculiar  lobulated  enlargement  of  the 
abdomen  develops,  characterized  by  a 
remarkable  globular  protrusion  and 
sagging  at  the  base,  and  by  unusual  depth  of  the  lateral  cutaneous 
creases.  Enteroptosis  is  very  commonly  associated  with  downward 
displacement  and  unnatural  mobility  of  the  kidneys,  and,  less  com- 
moaly,  of  the  liver  and  spleen. 


Fig.   201. — The  enteroptptic  ab- 
domen (Jefferson  Hospital). 


LOCAL  ABDOMINAL  ENLARGEMENTS 

In  dealing  with  circumscribed  enlargements  of  the  abdomen,  their 
general  situation,  whether  in  an  upper,  lower,  central,  or  lateral  zone 
of  the  belly,  should  be  determined  first,  and  then,  for  the  sake  of 
greater  accuracy,  their  more  precise  relation  to  one  of  the  arbitrary 
regions  lying  between  the  costal  arch  and  the  pubes.  In  such  local- 


PHYSICAL   DIAGNOSIS 


izations,  however,  no  hard  and  fast  lines  of  demarcation  are  possible, 
since  swellings  occupying  one  region  must,  by  their  evolution,  sooner 
or  later  tend  to  encroach  upon  neighboring  areas.  For  example,  the 
splenomegaly  and  hepatic  tumor  of  Band's  disease  primarily  cause 
bulging  below  the  costal  arch,  but  ultimately  the  visceral  enlargements 
distend  the  greater  part  of  the  abdomen,  extending  downward  to  the 
umbilicus,  and  perhaps  into  the  iliac  fossae  and  pelvis.  It  is  the 
origin  of  the  swelling  then,  rather  than  its  actual  site,  which  is  the 
important  point  to  remember  in  studying  a  local  abdominal  enlarge- 
ment. 

Enlargements  of  the  upper  abdomen  below  the  right  costal  arch  are 
suggestive  of  lesions  of  the  liver  and  gall-bladder — hepatoptosis, 
congestion,  cirrhosis,  amyloid  disease,  malignant  and  gummatous 
tumors,  echinococcus  cyst,  and  abscess  of  the  liver;  and  lithiasis, 
empyema,  or  cancer  of  the  gall-bladder.  Or  a  swelling  here  may  be 
due  to  a  fecal  or  a  malignant  tumor  of  the  ascending  colon  in  the 
neighborhood  of  the  hepatic  flexure.  Right-sided  subphrenic  pyo- 
pneumothorax  may  produce  an  immobile  mass  in  the  hepatic  region 


Fig.  202. — Epigastric  tumor  in  a  case  of  gastric  cancer  (Jefferson  Hospital). 

and  perhaps  in  the  epigastrium,  and  less  commonly  a  distention  of 
the  upper  right  abdomen  is  traceable  to  nephroptosis,  to  an  enlarged 
kidney,  or  to  retroperitoneal  adenitis. 

Enlargements  of  the  epigastrium  are  referable  chiefly  to  a  distended 
or  a  dilated  stomach,  and  to  neoplasms  of  the  pylorus,  left  lobe  of 
the  liver,  pancreas,  transverse  colon,  and  omen  turn.  Aneurism  of 
the  abdominal  aorta  is  recognized  as  a  pulsatile  tumor  in  the  median 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     51! 

line  of  the  epigastrium.  To  the  right  of  this  line  an  enlarged  gall- 
bladder may  be  detected,  and  to  the  left,  immediately  above  the  colon, 
an  effusion  into  the  lesser  peritoneal  sac.  Indurated  masses  in  the 
epigastrium  may  prove  to  be  retroperitoneal  or  mesenteric  glands 
enlarged  by  tuberculosis,  malignant  disease,  or  pseudoleukemia. 

Enlargements  below  the  left  costal  arch  may  indicate  splenomegaly, 
splenoptosis,  gastric  dilatation,  or  cancerous  growths  near  the  splenic 
flexure  of  the  colon.  Here  also  is  the  site  of  a  left-sided  subphrenic 
pyopneumothorax,  of  an  effusion  in  the  lesser  peritoneum,  and,  occa- 
sionally, of  renal  tumor  and  nephroptosis. 

Local  enlargements  in  either  flank  commonly  depend  upon  lesions 
of  the  uterus  and  adnexa — pyosalpinx,  ovarian,  uterine,  and  ligament- 
ous  tumors,  and  ectopic  gestation;  or  a  mass  in  one  of  the  iliac  areas 
may  mean  tuberculosis  or  malignant  disease  of  the  peritoneum, 
retroperitoneal  growths,  intussusception,  renal  tumor,  or  nephroptosis. 
A  psoas  abscess  may  bulge,  fluctuate,  and  point  in  the  groin  either 
below  or  above  Poupart's  ligament,  while  an  iliac  abscess  commonly 
appears  above  the  outer  end  of  this  landmark.  The  right  flank, 
at  or  near  McBurney's  point,  is  the  common  site  of  the  pal- 
pable tumor  of  appendicitis,  and  in  this  region  also  may  be  found 
the  tumors  due  to  neoplasms  of  the  cecum  or  ascending  colon  and 
to  fecal  impaction  in  these  portions  of  the  intestines.  In  the  left 
flank  similar  obstructive  lesions  of  the  descending  colon  and  sigmoid 
flexure  are  possible  causes  of  a  local  swelling,  additional  factors  to 
be  borne  in  mind  being  splenomegaly  and  splenoptosis. 

In  the  region  of  the  umbilicus,  a  distention  is  suggestive  of  gastric 
dilatation  and  displacement;  less  commonly,  of  enteroptosis  or  of 
other  visceral  ptoses — a  displaced  spleen  or  kidney  may  be  more 
conspicuous  near  the  navel  than  it  is  in  the  epigastrium  or  in  the 
flanks.  The  umbilical  region  is  also  the  site  of  hernia  and  of  the 
tumors  caused  by  tuberculous  peritonitis,  and  by  neoplasms  of  the 
stomach,  gut,  omentum,  and  mesentery.  In  this  region  also  appears 
most  conspicuously  the  cup-shaped  roof  of  the  dome-like  abdomen 
of  ruptured  extra-uterine  pregnancy,  described  by  Shulman. 

Distention  of  the  lower  abdomen  above  the  pubes,  if  not  obviously 
a  sign  of  pregnancy,  may  mean  an  overdistended  bladder  or,  very 
rarely,  physo-  or  hematometra.  Additional  factors  of  hypogastric 
swellings  include  the  above-noted  diseases  of  the  female  genital  organs, 
the  appendix,  and  the  peritoneum,  as  well  as  inguinal  hernia. 

On  inspection  massive  abdominal  tumors  may  account  for  an  appar- 
ent general  enlargement  of  the  abdomen,  but  by  careful  palpation 
and  percussion  such  growths  are  traceable  to  a  local  origin — visceral, 
peritoneal,  or  glandular.  It  is  especially  the  ovarian  cyst,  the  preg- 


512  PHYSICAL   DIAGNOSIS 

nant  or  fibroid  uterus,  the  leukemic  spleen,  the  overfull  bladder, 
and  the  cancerous  gut  and  peritoneum  which  at  first  glance  simulate 
a  universal  abdominal  distention.  In  addition  to  these  factors  many 
others  responsible  for  the  various  local  enlargements  mentioned  else- 
where may,  if  exaggerated,  also  cause  an  apparent  general  dis- 
tention. 

In  the  distention  due  to  an  ovarian  cyst  the  dome  of  the  abdomen 
gives  a  dull  percussion  sound  while  the  flanks  on  either  side  are  tym- 
panitic,  these  signs  persisting  when  the  subject  turns  from  the  dorsal 
to  the  lateral  decubitus.  The  same  is  true  of  the  gravid  uterus  and 
of  uterine  fibroid.  In  differentiating  these  three  conditions,  vaginal 
examination,  the  cautious  use  of  the  aspirator,  and  the  history  of 
the  patient  are  important  diagnostic  adjuncts.  A  leukemic  spleen 
may  be  readily  mapped  out  by  palpation  and  by  the  dulness  -over 
the  upper  and  sometimes  the  lower  left  abdominal  region,  and  in 
this  disease  the  blood  count  is  pathognomonic.  The  distended 
bladder  forms  a  dull  area  encircled  by  a  tympanitic  zone  in  the  lower 
mid-abdomen,  which  findings,  it  need  scarcely  be  noted,  vanish  after 
catheterization.  In  the  cancerous  intestines  and  peritoneum  the  resist- 
ant, nodular  character  of  the  growths,  their  asymmetric  distribu- 
tion, and  perhaps  the  presence  of  metastatic  tumors  furnish  the 
important  clues. 

ABDOMINAL  MOVEMENTS 

The  various  movements  of  the  abdomen  to  be  noted  on  inspection 
relate  to  the  respiratory  excursions,  to  local  areas  of  pulsation,  and  to 
peristalsis  of  the  stomach  and  intestines.  Exaggerated  abdominal 
movements  during  respiration  are  generally  due  to  some  thoracic 
lesion  which  restricts  the  normal  rise  and  fall  of  the  diaphragm.  En- 
feeblement  of  such  movements  occurs  as  the  effect  of  abdominal  dis- 
tention, pain,  and  paralysis,  as,  for  instance,  in  ascites,  meteorism, 
and  tumors,  in  peritonitis,  and  in  paralysis  of  the  abdominal  muscles. 
These  causes,  together  with  those  of  local  pulsations  in  the  epigastrium 
have  already  been  considered.  (See  Anomalies  of  Respiration,  p. 
95,  and  Abnormal  Areas  of  Pulsation,  p.  321.)  Here  may  be  men- 
tioned the  rhythmic  throbbing  near  the  umbilicus,  occasionally 
symptomatic  of  acute  enteritis  (Stokes) . 

Peristalsis  of  the  stomach  and  gut  may  be  visible  under  normal 
conditions  in  subjects  with  thin,  flaccid  abdominal  walls,  but  more 
often  it  is  a  sign  of  marked  gastric  dilatation,  perhaps  with  pyloric 
obstruction,  or  of  stenosis  of  the  intestine,  with  dilatation  above  the 
point  of  constriction.  Exaggerated  peristalsis  also  may  be  seen 
in  overdistention  of  the  gut  associated  with  enteritis  and  with  the 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     513 


functional  neuroses.  Kussmaul's  "peristaltic  unrest"  is  simply  an 
excessive  peristalsis,  betrayed  by  volleys  of  gurgles  and  rumbles 
of  flatus  (borborygmi) ,  and  chiefly  affecting  women  whose  neurotic 
temperament,  tight  stays,  and  overeating  account  for  these  embarrass- 
ing echoes.  Visible  peristalsis  appears  as  a  succession  of  undulatory 
movements  travelling  with  a  sort  of  worm-like  motion  across  the 
belly — from  left  to  right,  if  the  peristalsis  be  of  the  stomach,  and  from 
right  to  left,  if  it  be  of  the  intestines.  Peristalsis  of  the  stomach  is 
seen  best  in  the  epigastrium ;  of  the  large  intestine,  in  the  epigastrium 
and  in  the  right  or  left  flank,  according  to  which  section  of  the  tube, 
transverse,  ascending,  or  descending,  be  affected;  and  of  the  small 
intestines,  in  the  region  of  the  umbilicus.  In  this  situation  a  circum- 
scribed area  of  peristaltic  gut,  massed  together  coil  upon  coil,  suggests 
stenosis  at  or  near  the  ileocecal  valve. 

THE  SKIN  AND  SUBCUTANEOUS  TISSUES 

The  nutrition  of  the  skin  and  structures  beneath  suffers  decidedly 
in  many  wasting  diseases,  as  examples  of  which  may  be  cited  tuber- 
culous peritonitis,  malignant 
disease  of  the  abdominal  vis- 
cera, and  Asiatic  cholera.  In 
such  conditions,  in  addition  to 
obvious  wasting  of  the  abdom- 
inal wall,  the  skin  is  dry,  fur- 
furaceous,  bloodless,  and  so  in- 
elastic that  it  may  be  pinched 
up  and  molded  between  the 
fingers  like  a  ball  of  putty.  In 
advanced  senility  and  in  the 
multipara  the  abdominal  pari- 
etes  are  thin,  toneless,  and  re- 
laxed, and  as  the  effect  of  long- 
continued  distention  the  skin 
of  the  abdomen  becomes  tense, 
shiny,  preternaturally  dry,  and 
even  duskily  blue  in  the  de- 
pendent parts  of  the  flanks. 
Increased  thickness  of  the  ab- 
dominal wall  may  be  muscular, 

fatty,    Or    edematOUS.      Edema      Fig- 203.— Venous  engorgement  of  the  ab- 
,     i  .  .  ,  dommal  wall   (Jefferson  Hospital). 

ot  this  region  is  recognized  as 

a  boggy  thickening  which  pits  upon  pressure  like  a  soft  apple,  es- 
pecially in  the  flanks  and  loins;  it  is  commonly  part  of  the  anasarca 
33 


514  PHYSICAL   DIAGNOSIS 

of  renal  or  cardiac  disease,  and  may  or  may  not  be  associated  with 
ascites.  Angioneurotic  edema  occasionally  attacks  the  abdominal 
wall,  appearing  as  an  ephemeral  local  tumefaction,  too  tense  to 
pit  deeply  and  either  blanched  or  of  a  scarlet  hue.  In  the  excep- 
tional instance  diffuse  purulent  infiltration  may  account  for  a 
widespread  edematous  thickening  of  the  abdominal  parietes. 

As  types  of  color  changes  in  the  skin  of  the  abdomen  and  elsewhere 
there  are  to  be  recalled  the  saffron  discoloration  of  icterus;  the  blue 
mottling  of  cyanosis;  the  dark  pigmentation  of  Addison's  disease, 
peritoneal  tuberculosis,  argyria,  and  vagabondism;  the  dirty  brown 
or  yellow  patches  of  tinea  versicolor;  and  the  coppery  macular  areas 
of  syphilis.  Multiple  white,  silvery,  or,  rarely,  pigmented  linear 
markings  upon  the  abdomen  may  have  been  caused  by  pregnancy, 
ascites,  and  various  causes  of  chronic  abdominal  distention;  gener- 
ically,  these  streaks  are  designated  as  linece  albicantes,  or,  if  due  to  preg- 
nancy, as  linece  gravidarum.  The  appearance  of  a  white  line  upon 
the  skin  of  the  abdomen  (ligne  blanche  abdominale)  after  friction 
with  a  blunt  instrument  is  described  by  Sargent  as  an  occasional 
finding  in  suprarenal  insufficiency.  Scars,  aside  from  those  due  to 
accidents  and  to  operations,  may  be  the  relic  of  a  previous  attack 
of  syphilis,  of  a  chancroidal  bubo,  or  of  a  destructive  skin  dis- 
ease. Venereal  infection,  tuberculosis,  malignant  disease,  and  in- 
jury by  a  sudden,  violent  strain  are  suggested  when  enlarged 
glands  are  discovered  in  the  groin.  Small,  steel-gray  points  of  fat 
necrosis  are  sometimes  perceptible  in  cases  of  pancreatitis,  and 
hard  subcutaneous  nodules  may  develop  just  beneath  the  skin  in 
sarcomatosis  and  in  cancer  of  the  abdominal  organs. 

Enlarged  and  tortuous  veins  coursing  over  the  abdomen  are  a  valu- 
able sign  of  venous  obstruction,  and  generally  mean  Laennec's  cir- 
rhosis, although  less  commonly  they  result  from  portal  vein  throm- 
bosis, ascites,  or  pressure  by  neoplasms  upon  the  superior  or  inferior 
vena  cava.  The  caput  Medusae  of  the  gin-liver  consists  of  a  bunch 
of  tortuous  venules  about  the  navel,  and  indicates  portal  obstruction, 
as  the  result  of  which  there  has  been  established  a  compensatory 
anastomosis  between  a  para-umbilical  vein  and  the  superior  epigastric 
veins  (Sappey) .  By  making  pressure  upon  an  abnormally  dilated 
abdominal  vein  it  is  possible  to  determine  whether  the  obstruction 
involves  the  superior  or  the  inferior  vena  cava;  if  it  be  the  former,  the 
vein  distends  above  the  point  of  pressure,  while  if  it  be  the  latter, 
the  fulness  appears  below  the  constriction.  The  flow  within  the 
enlarged  veins  radiating  from  the  navel  is  away  from  this  point. 

Umbilical  Changes. — The  condition  of  the  navel  is  not  only  a  good 
index  of  the  thoroughness  of  one's  personal  hygiene,  but  a  collateral 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     515 

sign  of  clinical  moment.  In  an  overfat  abdomen  the  navel  is  retracted 
perhaps  to  the  point  of  obliteration;  it  protrudes  conspicuously  in 
late  pregnancy,  umbilical  hernia,  and  portal  obstruction;  and  it  is 
stretched  and  depressed  in  the  abdominal  fulnesses  of  early  preg- 
nancy, ascites,  and  new-growths.  The  navel  may  be  the  seat  of 
inflammation  and  eczema,  and  in  congenital  umbilical  fistula  it  may 
ooze  a  clear  serous  fluid.  F.  P.  Henry  regards  peri-umbilical  ery- 
thema as  an  important  diagnostic  sign  in  tuberculous  peritonitis. 
A  malignant  neoplasm  of  the  liver  may  rigidly  immobilize  the 
umbilicus. 

Muscular  Rigidity. — Increased  resistance  to  pressure  and  actual 
spontaneous  rigidity  of  the  abdominal  musculature  are  suggestive  of 
either  peritoneal  irritation  or  inflammation.  General  rigidity  of  the 
belly  wall  is  met  with  in  acute  general  peritonitis,  but  a  practically 
similar  spasm  also  attends  certain  inflammations  above  the  dia- 
phragm, particularly  croupous  pneumonia  and  diaphragmatic  pleu- 
risy. Local  muscular  rigidity  may  point  definitely  to  an  inflamma- 
tory lesion  of  one  of  the  abdominal  organs — to  appendicitis  or  to 
extensive  typhoid  ulceration,  if  it  affects  the  right  iliac  region;  to 
perisigmoid  inflammation,  if  it  be  in  the  left  iliac  space;  to  chole- 
lithiasis, gastric  ulcer,  or  pancreatitis,  if  it  be  epigastric. 

FLUCTUATION 

The  palpating  hand  seldom  appreciates  any  decided  tactile  differ- 
ences in  the  resistance  of  the  gaseous  and  the  liquid  strata  of  an  ascitic 
abdomen,  but  fluctuation,  a  certain  sign  of  fluid,  is  demonstrable  if 
a  moderately  large  effusion  be  present.  To  obtain  this  sign  the 
examiner  palpates  one  flank  and  gently  but  sharply  taps  with  the 
finger-tips  the  opposite  side  of  the  abdomen,  an  assistant  meanwhile 
pressing  firmly  with  his  hand  held  edgewise  in  the  median  line,  so 
as  to  cut  off  the  vibrations  of  the  abdominal  wall.  If  fluid  be  present 
a  distinct  jog,  due  to  a  wave  of  liquid  set  in  motion  by  the  percussion, 
is  felt  by  the  palpating  palm.  Ascites  does  not  invariably  give  this 
sign,  for  it  may  be  impossible  to  agitate  a  liquid  wave  both  in  very 
slight  and  in  very  extensive  dropsical  accumulations.  The  percussion 
findings  associated  with  this  tactile  sign  of  intraperitoneal  fluid  are 
described  on  p.  506. 

Fluctuation  of  an  abdominal  mass  indicates  encysted  fluid.  The 
sign  may  obviously  relate  also  to  an  iliac  abscess  or  to  an  abscess  of  the 
abdominal  wall.  In  other  instances  it  is  attributable  to  a  distended 
bladder;  to  pregnancy,  normal  or  extra-uterine;  to  ovarian,  tubal, 
hepatic,  or  renal  cyst  or  abscess;  and  to  general  effusions  in  the  lesser, 
and  encysted  effusions  in  the  greater,  peritoneum. 


516  PHYSICAL   DIAGNOSIS 

TACTILE  FRICTION  AND  THRILLS 

In  tuberculous  peritonitis  coarse  tubercle  friction,  due  to  the  rubbing 
together  of  peritoneal  tubercles,  is  sometimes  elicited  by  kneading 
the  abdomen  with  the  finger  tips.  In  other  forms  of  peritonitis, 
especially  the  chronic,  fine  peritoneal  friction  is  occasionally  felt 
over  the  upper  part  of  the  abdomen.  Over  the  liver  a  palpable 
friction-rub  during  respiration  suggests  perihepatitis,  secondary 
to  hepatic  abscess  or  cancer,  or  developing  by  the  extension  of 
pleurisy  or  of  peritonitis.  Subphrenic  peritonitis  likewise  ac- 
counts for  tactile  friction  in  this  area.  Rarely,  inflammation  of 
the  peritoneal  covering  of  the  spleen  causes  a  similar  rub  over  the 
splenic  area.  Perihepatitic  and  perisplenitic  friction  are  most  dis- 
tinctly felt  during  full  inspiration  and  disappear  when  adhesions 
form  between  the  affected  organs  and  the  abdominal  wall.  Chole- 
lithiasis may  underlie  two  tactile  signs  localized  to  the  region  of  the 
gall-bladder:  palpable  friction  with  respiration,  excited  by  local 
inflammation  of  the  peritoneum  at  the  gall-bladder  and  of  the  adja- 
cent hepatic  peritoneal  reflection  (Gerhardt) ;  and  a  grating  gall-stone 
crepitus,  due  to  friction  of  the  calculi  by  palpatory  manipulation. 

Xiphoid  crepitation,  a  tactile  sensation  akin  to  that  of  emphyse- 
matous  crackling,  is  described  by  Galvagni  as  an  evidence  of  peri- 
tonitis. It  is  elicited  by  pressure  over  the  xiphoid  tip  and  the  upper 
.  costal  arch,  and  is  explained  by  the  mechanical  separation  of  perito- 
neal adhesions,  as  well  as  by  the  presence  of  subcutaneous  bullae 
created  by  gas-forming  bacteria. 

A  palpable  thrill  in  the  epigastrium,  with  visible  throbbing  of  a 
tumor,  giving  expansile  pulsation  and  a  systolic  murmur,  is  found  in 
aneurism  of  the  abdominal  aorta.  Over  an  accessible  hydatid 
cyst  the  so-called  hydatid  thrill  or  fremitus  can  be  sometimes 
detected  by  palpatory  percussion.  (See  p.  135.) 

PAIN  IN  THE  ABDOMEN 

It  is  important  to  bear  in  mind  that  abdominal  tenderness  and 
pain  relate  not  only  to  lesions  of  the  abdomen,  but  also  to  disorders 
elsewhere  situated,  notably  those  affecting  the  thoracic  organs  and 
the  spine.  The  acutely  painful  abdomen  of  pneumonia  and  the 
excruciating  gastric  crises  of  tabes  dorsalis  are  two  striking  illus- 
trations of  pain  reflected  to  the  abdomen  from  remote  regions, 
the  examination  of  which  should  not  be  neglected  in  attempting  to 
discover  the  true  cause  of  a  tender  or  an  aching  belly.  Furthermore, 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     517 


diseases  of  the  abdominal  organs  frequently  account  for  pain  in  re- 
gions far  removed  therefrom,  as  in  the  shoulder  pains  symptomatic 
of  lesions  of  the  liver  and  colon,  in  the  tender  spine  of  gastric 
ulcer,  and  in  the  painful  testicle  of  stone  in  the  kidney. 

Generalized  abdominal  tenderness  and  pain  usually  is  traceable  to  such 
conditions  as  gastro-intestinal  disease,  meteorism,  peritonitis,  irritant 
poisons,  abdominal  myalgia,  or  hysteria.  Or  when  diffused  through- 


Gall-bladder  disease 
Robson's  point 

4 

Intussusception 
McBurney's  point  - 

Clado's  point 
Ureteral  disease 


Gastric  ulcer 


Morris's  poin 


points 


Volvulus 


Fig.  204. — i.  Diseases  of  stomach,  gall-bladder,  duodenum,  transverse  colon,  and 
pancreas;  abdominal  aneurism;  pneumonia;  phrenic  pleurisy;  pericarditis;  appendicitis; 
diabetes;  uremia;  eclampsia.  2.  Diseases  of  stomach,  splenic  colon;  enteroptosis, 
nephroptosis,  nephralgia.  3.  Diseases  of  intestines,  omentum,  mesentery,  and  perito- 
neum; lead  colic;  abdominal  arteriosclerosis.  4.  Diseases  of  liver,  hepatic  colon,  and 
right  kidney.  5.  Diseases  of  spleen,  splenic  colon,  and  left  kidney.  6.  Diseases  of 
urinary  bladder  and  pelvic  organs. 


out  the  abdomen  it  may  stand  for  the  radiation  of  pain  originating  in 
one  of  the  abdominal  viscera  or  in  some  extra-abdominal  structure, 
as  in  renal  colic,  appendicitis,  dysmenorrhea,  and  diaphragmatic 
pleurisy,  in  which  the  pain,  primarily  circumscribed  to  the  local 
lesion,  secondarily  spreads  far  beyond  its  original  confines.  Cir- 
cumscribed tenderness  and  pain  should  be  investigated  with  refer- 
ence to  its  origin  in,  and  reflection  from,  the  organs  and  other  struct- 


5l8  PHYSICAL   DIAGNOSIS 

ures  corresponding  to  the  several  surface  divisions  of  the  abdominal 
wall,  the  findings  thus  obtained  being  interpreted  in  the  light  of  a 
full  clinical  inquiry  by  other  methods  of  examination  (Fig.  204). 

Pain  in  the  epigastrium  ordinarily  is  of  purely  gastric  origin,  as  in 
neuralgia,  inflammation,  ulcer,  or  cancer  of  the  stomach,  but  to  this 
region  the  pain  of  diseases  of  the  gall-bladder  and  gall-ducts  also  is 
commonly  referred.  In  cholecystitis  deep  tenderness  may  be  in- 
duced at  the  end  of  full  inspiration  if  the  examiner's  fingers  be  thrust 
upward  beneath  the  costal  arch  at  the  outer  limit  of  the  right  epi- 
gastrium— Naunyn's  sign.  Epigastric  pain  may  be  symptomatic  of 
duodenal  ulcer  or  of  an  impacted  transverse  colon;  of  some  pancreatic 
lesion,  such  as  inflammation,  hemorrhage,  or  carcinoma;  of  circum- 
scribed peritonitis;  of  aneurism  of  the  abdominal  aorta;  of  myalgia 
of  the  abdominal  musculature;  or  of  vertebral  disease.  It  is  also  to 
be  recalled  that  severe  epigastric  pain  is  a  common  complaint  in 
infantile  pneumonia,  diaphragmatic  pleurisy,  pericarditis,  and  rheu- 
matic fever;  and  that  it  frequently  accompanies  visceroptosis  and 
appendicular  inflammation.  Severe  crises  of  epigastric  pain  are  a 
well-known  premonitory  sign  of  diabetic  coma,  and  less  commonly 
accompany  other  intoxications,  notably  uremia  and  eclampsia. 

Pain  in  the  umbilical  region,  if  not  traceable  to  some  one  of  the 
conditions  just  enumerated,  may  be  indicative  of  enteritis,  enteralgia, 
intestinal  obstruction  or  ulceration,  lead  colic,  general  peritonitis, 
omental  carcinoma,  or  mesenteric  cyst.  Here  also  may  be  the  seat 
of  pain  in  abdominal  arteriosclerosis,  angina  pectoris,  ureteritis, 
and  embolism  of  the  superior  mesenteric  artery.  The  girdle  pain 
of  locomotor  ataxia,  myelitis,  and  spinal  meningitis  encircles  the 
body,  as  a  painful  sense  of  constriction,  in  the  upper  part  of  the 
umbilical  rectangle.  Two  diagnostic  points  of  pain  on  pressure  are 
also  situated  in  this  area  of  the  abdomen:  Mayo  Robson's  point,  at 
the  junction  of  the  outer  and  middle  third  of  a  line  drawn  from  the 
ninth  costal  cartilage  to  the  umbilicus,  where  tenderness  indicates 
inflammatory  lesions  of  the  gall-bladder  and  ducts;  and  Morris's  point 
of  tenderness  in  appendicitis,  situated  \\  inches  (3.75  cm.)  from  the 
navel  on  a  line  running  thence  to  the  right  anterior  superior  iliac 
spine.  Tenderness  at  this  point  and  also  at  a  corresponding  point 
to  the  left  of  the  navel  suggests  pelvic,  not  appendical,  disease,  in 
which  the  sensitiveness  is  right  sided  only. 

Hypogastric  pain  relates  principally  to  diseases  of  the  urinary  blad- 
der, of  which  cystitis  in  particular,  and  also  acute  distention,  calculus, 
tuberculosis,  and  neoplasm  are  accredited  causes.  In  women  uterine 
and  ovarian  disease,  pelvic  inflammation,  and  ectopic  gestation  are 


EXAMINATION   OF   ABDOMEN  AND   ABDOMINAL  VISCERA     519 

also  to  be  reckoned  with  as  possible  factors  of  pain  above  the 
pubes  and  in  the  lateral  regions  bordering  thereupon.  Voillemier's 
point,  selected  as  the  site  for  puncturing  a  distended  bladder,  is 
situated  in  the  linea  alba  2^  inches  (6.25  cm.)  below  the  interspinal 
line. 

Either  ileolumbar  region  may  be  the  seat  of  maximum  tenderness 
in  abdominal  pain  due  to  colitis,  hernia,  varicocele,  renal  colic, 
floating  kidney,  or  ovaritis.  On  the  right  side  pain  is  suggestive 
particularly  of  intussusception,  cecal  impaction,  enteric  fever,  and 
appendicitis;  while  left-sided  pain  in  this  area  may  indicate  volvulus, 
sigmoid  impaction,  or  pericolitis  sinistra.  McBurney's  point  of 
appendical  pain  is  situated  in  the  right  iliac  region  \\  inches  (3.75 
cm.)  from  the  anterior  superior  iliac  spine  on  a  line  drawn  from 
this  prominence  to  the  umbilicus,  dado's  point,  having  a  similar 
significance,  lies  at  the  intersection  of  the  right  semilunar  line  by 
the  interspinal  line  at  the  external  border  of  the  rectus  abdominis 
muscle. 

Pain  in  the  hypochondriac  regions  and  in  the  loins  and  sacrum 
has  been  dealt  with  in  Section  II.  (Seep.  120.) 

EXAMINATION  OF  THE  STOMACH 

Clinical  Anatomy. — The  stomach  occupies  the  left  hypochon- 
drium  and  part  of  the  epigastrium,  lying  chiefly  to  the  left  of  the 
median  line  in  an  almost  vertical  position,  with  the  subject  in  the 
erect  posture  (Fig.  205).  The  old  conception  of  the  stomach's 
transverse  position  in  the  upper  abdominal  cavity  must  be  revised 
by  the  newer  truths  of  modern  radiography,  which  shows  radical 
differences  in  the  topography  of  the  organ  according  to  the  in- 
fluences of  posture,  degree  of  distention,  and  amount  of  contained 
food.  When  empty  and  contracted  the  stomach  is  represented  by 
a  small  pyriform  sac  filled  with  gas,  and  situated  beneath  the  left 
dome  of  the  diaphragm.  This  communicates  with  a  collapsed 
tubular  structure  whose  opposed  walls  for  the  greater  part  conform 
to  the  vertical  plane  of  the  body  except  near  the  midline,  where 
they  run  almost  horizontally.  When  fully  distended  the  stomach 
is  comparable  in  shape  to  an  elongated  gourd  of  virtually  uniform 
diameter  following  the  vertical-oblique  course  above  indicated. 

The  cardia,  or  gastro-esophageal  orifice,  corresponds  anteriorly 
to  a  point  on  the  seventh  left  costal  cartilage  i  inch  (2.5  cm.) 
from  the  sternum,  and  posteriorly  to  the  level  of  the  ninth  thoracic 
vertebra.  The  pylorus,  or  gastroduodenal  opening,  unlike  the 


520  PHYSICAL   DIAGNOSIS 

cardia,  is  freely  movable,  and  is  situated,  when  the  stomach  is 
empty,  in  the  median  line  3  or  4  inches  (7.5  to  10  cm.)  below  the 
xiphisternal  junction,  but  when  the  stomach  is  distended  the 
pylorus  moves  2  or  3  inches  (5  to  7.5  cm.)  to  the  right  of  the  median 
line;  posteriorly,  the  pylorus  is  opposite  the  first  lumbar  vertebra. 
The  pyloric  region  also  includes  a  vestibule,  directed  upward  to  the 
right  of  the  median  line,  and  a  canal,  running  thence  upward,  back- 
ward, and  toward  the  right  to  project  into  the  duodenum.  The 
Addison-Cunningham  transpyloric  line,  crossing  the  belly  midway 


Fig.  205. — Surface  topography  of  the  stomach,  when  empty  (inner  broken  outline), 
and  in  full  distention  (outer  solid  outline). 

between  the  suprasternal  notch  and  the  pubic  symphysis,  bisects 
the  pyloric  end  of  the  stomach.  Thefundus,  or  the  rounded  dome 
of  the  stomach  to  the  left  of  the  cardia,  lies  behind  and  somewhat 
to  the  left  of  the  heart's  apex,  and  occupies  the  left  vault  of  the 
diaphragm.  The  body,  lying  entirely  to  the  left  of  the  median 
line,  is  situated  either  vertically  or  somewhat  obliquely  toward 
the  right,  according  to  the  position  of  the  trunk,  whether  upright 
or  recumbent.  The  lesser  curvature,  or  the  upper  concave  border 
of  the  stomach,  lies  in  the  epigastric  region,  deeply  situated  be- 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     521 

neath  the  lower  border  of  the  liver.  In  general,  its  course  corre- 
sponds to  that  of  the  opposed  wall  of  the  empty  contracted  stom- 
ach. A  distinct  depression  on  the  lesser  curvature,  the  incisura 
angular  is,  separates  the  body  from  the  pyloric  portion.  The 
greater  curvature,  or  the  lower  convex  border  of  the  stomach,  lies 
beneath  the  ninth  costal  cartilage  at  the  left  costal  arch,  and  is 
situated  at  or  slightly  below  the  umbilicus  in  the  median  line  of 


Fig.  2050. — Radiograph  of  the  normal   stomach  in  a  state  of  complete  distention. 
Cf.  Figs.  206  and  207.     (Plate  by  Dr.  W.  F.  Manges.) 

the  abdomen.     In  children  it  is  generally  much  lower,  even  below 
the  level  of  the  iliac  crests. 

Inspection. — Aside  from  the  detection  of  peristalsis  and  of  pul- 
sating areas  in  the  epigastrium,  previously  described  (p.  324) ,  inspec- 
tion of  the  gastric  region  is  useful  in  determining  the  size  and  the 
position  of  the  stomach.  In  the  thin  subject  it  is  sometimes  possible 
to  perceive  the  contour  of  the  greater  curvature  and  its  respiratory 
rise  and  fall,  even  if  the  stomach  be  but  moderately  distended,  and 
the  outline  of  the  lesser  curvature  may  be  visible  if  the  organ  be 


522  PHYSICAL   DIAGNOSIS 

greatly  depressed.  In  other  instances  it  is  necessary  to  inflate 
the  stomach,  either  with  air  by  means  of  a  bulb-syringe,  or  with 
carbon  dioxid  evolved  from  sodium  bicarbonate  and  tartaric  acid.1 
Artificial  distention  of  the  stomach  may  reveal  a  pyloric  tumor 
otherwise  invisible,  while  a  phantom  tumor  due  to  a  tightly  con- 
tracted gastric  musculature  promptly  disappears  when  the  stomach 
is  inflated. 

When  a  patient  whose  stomach  is  dilated  and  displaced  stands 
erect,  the  epigastrium  becomes  distinctly  concave,  and  the  lower 
central  and  lateral  regions  of  the  belly  bulge  forward  and  sag  down- 
ward in  the  form  of  a  flaccid  globular  mass  bounded  on  either  flank 
by  a  deep  sulcus  running  obliquely  downward  toward  the  pubis 
from  the  iliac  crests.  In  the  dorsal  decubitis  the  epigastric  hollow 
becomes  shallower,  the  abdominal  prominence  flattens,  and  the 
enlargement  of  the  flanks  is  more  conspicuous.  (Cf.  Figs.  200  and 
201.) 

Inasmuch  as  an  enlarged  stomach  extends  chiefly  in  a  downward 
direction,  the  lower  border  is  taken  as  a  clinical  index  of  the  organ's 
size  and  site.  A  lower  border  well  below  the  navel  may  safely  be 
regarded  as  symptomatic  of  either  dilatation  or  of  displacement,  for 
the  differentiation  of  which  other  data  are  essential.  In  gastrec- 
tasis  the  pylorus  is  but  slightly  lower  than  its  normal  site  below  the 
right  costal  arch,  the  distance  between  the  two  curvatures  of  the 
stomach  is  greatly  increased,  and  the  lower  border  is  depressed  to 
the  level  of  the  navel  or  somewhat  below  it;  while  in  gastroptosis 
the  pylorus  occupies  the  umbilical  region,  the  distance  between 
the  stomach's  curvatures  is  approximately  normal,  and  the  lower 

1  Mechanical  inflation  requires  the  introduction  of  a  stomach-tube,  to  the 
buccal  end  of  which  is  coupled  a  Davidson  syringe,  which  is  then  manipulated 
until  sufficient  air  has  been  pumped  into  the  stomach.  By  this  procedure  the 
amount  of  gastric  distention  may  be  exactly  controlled  and  the  distressing 
symptoms  of  overinflation  quickly  relieved  ;  it  is,  however,  objectionable  in 
patients  to  whom  the  passage  of  the  tube  is  a  trying  ordeal,  if  not  a  positive 
danger.  Carbon  dioxid  inflation,  the  best  method  for  the  average  case,  is 
accomplished  by  giving  the  patient  a  dram  of  sodium  bicarbonate  dissolved  in 
half  a  tumblerful  of  water,  followed  at  once  by  a  dram  of  tartaric  acid  sim- 
ilarly diluted.  The  carbonic  acid  gas  thus  evolved  in  the  stomach  quickly 
distends  the  organ  sufficiently  for  a  satisfactory  examination.  This  process  of 
chemical  inflation  has  been  criticized  chiefly  because  the  gas  generation  can- 
not be  controlled,  and  hence  may  cause  cardiac  embarrassment  as  well  as 
active  gastric  distress  from  the  irritant  effects  of  the  effervescence.  Practi- 
cally, overdistention  is  promptly  relieved  by  the  escape  of  gas  through  the 
cardia,  whence  it  is  disposed  of  by  belching ;  or,  in  an  extremity,  the  tube  may 
be  passed  to  relieve  the  pressure. 

Organic  cardiac  disease,  recent  hematemesis,  gastric  ulcer  and  other  factors 
that  seriously  weaken  the  gastric  parietes  are  causes  of  possible  danger  in  infla- 
tion of  the  stomach  by  either  of  the  above  methods. 


EXAMINATION  OF   ABDOMEN  AND  ABDOMINAL  VISCERA     523 

border  lies  far  below  the  navel,  perhaps  almost  as  low  as  the  pubes. 
From  this  it  is  evident  that  the  site  of  the  pylorus,  and  not  simply 
the  position  of  the  lower  border  of  the  stomach,  is  the  criterion  in 
distinguishing  dilatation  and  displacement  of  the  organ.  These 
signs,  it  must  be  added,  are  always  to  be  supplemented  by  a  deter- 
mination of  the  stomach's  motor  powers  and  by  laboratory  tests. 
The  radiograph  on  this  page  (Fig.  206)  well  illustrates  the  size  and 


Fig.  206. — Radiograph  of  a  dilated^nd  displaced  stomach.   Cf.  Fig.  2050.   (Plate  by 

Dr.  W.  F.  Manges.) 

site  of  a  dilated  and  displaced  stomach.  The  striking  double 
sacculation  of  the  hour-glass  stomach  may  be  made  visible  by  infla- 
tion, and  in  this  rare  deformity  it  is  possible  to  trace  the  outline  of 
the  deeply  notched  lower  gastric  border  where  a  cicatricial  con- 
traction divides  the  stomach  into  two  separate  compartments,  one 
pyloric  and  the  other  cardiac,  which  communicate  by  a  narrow 
opening  (Fig.  207).'  An  hour-glass  stomach  usually  yields  by 
siphonage  less  fluid  than  has  been  poured  in  through  the  stomach- 
tube,  and,  though  apparently  drained  dry,  may  afford  a  sudden 
commingling  of  splashing  sounds  and  other  signs  indicating  the 
reappearance  of  fluid  in  the  empty  compartment. 


524  PHYSICAL   DIAGNOSIS 

X-ray  examination  of  the  stomach  is  most  useful  in  determining 
the  size,  contour,  position,  and  peristaltic  action  of  the  organ,  and, 
with  less  certainty,  the  existence  of  neoplasms.  The  best  results, 
both  from  radiography  and  from  radioscopy,  are  obtained  by  using 
the  rays  after  the  stomach  has  been  rendered  opaque  by  the  admin- 


Fig.  207. — Radiograph  of  an  hour-glass  stomach.   Cf.  Fig.  2050.    (Plate  by  Dr.  W.  F. 

Manges.) 

istration  of  i  pint  (480  cc.)  of  kefir,  of  mucilage  of  acacia,  or  of  thin 
gruel  containing  about  i  ounce  (31  gm.)  of  bismuth  sulphate. 

Bismuth  subnitrate,  owing  to  its  potential  toxicity  from  nitrite- 
poisoning,  has  been  generally  abandoned  in  favor  of  the  sulphate, 
carbonate,  or  oxid,  all  of  which  are  harmless.1  Within  from  four 

1  For  radiographic  examination  of  the  alimentary  canal  the  Royal  Society 
of  Medicine  recommends  standard  test-meals  of  porridge  and  of  bread  and 
milk,  each  to  be  incorporated  with  2  ounces  (62  gm.)  of  barium  sulphate  or 
of  bismuth  oxychlorid.  The  porridge  meal  is  prepared  by  adding  to  7  ounces 
(247  gm.)  of  fine  oatmeal  sufficient  milk  to  make  the  total  bulk  10  ounces 
(310  cc.),  sweetening  the  mixture  with  brown  sugar.  The  bread  and  milk  is 
made  by  mixing  2  ounces  (62  gm.)  of  soft  white  bread  with  8  ounces  (240  cc.) 
of  whole  or  malted  milk,  sugar  being  added  to  taste.  With  each  of  these  test- 
meals,  to  be  given  on  an  empty  stomach,  the  proper  quantity  of  bismuth  or 
barium  is  mixed  just  before  use. 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     525 

to  six  hours  after  the  ingestion  of  this  bismuth  test-meal  the  nor- 
mal stomach  shows  no  vestige  of  the  salt,  which  passes  through 
the  ileocecal  valve  into  the  colon  within  from  eight  to  ten  hours 
and  through  the  descending  colon  and  rectum  within  twenty-four 
hours.  Serial  radiographs  taken  immediately  after  the  patient 
swallows  the  bismuth  meal  and  twenty-four  hours  thereafter,  with 
exposures  made  at  two-hour  intervals  during  the  first  twelve 
hours,  provide  accurate  and  correlated  data  of  the  condition  of  the 
entire  gastro-intestinal  canal.  Especially  is  this  true  of  such  a 
series  supplemented  by  one  or  two  radiographs  of  the  colon  taken 
after  the  injection  of  a  suitable  clyster.  (See  p.  535.) 

By  combined  radiography  and  fluoroscopy  many  cases  of  cancer 
and  ulcer  of  the  stomach  are  differentiated  at  an  early  period  of  their 
development  chiefly  by  criteria  such  as  test-meal  residue,  pyloric 
patency,  and  irregularities  of  contour 

In  gastric  cancer  this  complex  is  sought  for:  antiperistalsis ;  un- 
natural patency  or  actual  obstruction  of  the  pylorus;  large  residue 
of  the  test-meal  after  six  hours;  fixation  of  the  stomach  as  a  whole; 
and  irregularities  of  contour  due  to  neoplastic  deformity.  In 
gastric  ulcer  it  may  be  possible  to  identify  the  projecting  shadow 
of  the  ulcerative  mass,  and  also  the  extragastric  cavity  caused  by 
the  extension  of  a  perforative  process  into  neighboring  tissues, 
hepatic  or  pancreatic.  Other  radiographic  signs  include  Indenta- 
tion of  the  gastric  wall  opposite  to  the  site  of  the  ulcer,  an  appre- 
ciable six-hour  residue  of  bismuth,  and  suggestive  defects  of  shape 
and  motility,  such  as  antiperistalsis,  delayed  pyloric  patency, 
hour-glass  constriction,  and  a  "fish-hook"  contour  of  the  entire 
stomach. 

Gastrodiaphany,  or  transillumination  of  the  stomach,  requires 
the  introduction  into  the  stomach  of  a  gastrodiaphane,  or  a  soft 
rubber  tube,  to  the  lower  end  of  which  is  attached  a  small  incan- 
descent lamp,  which  when  illuminated  renders  the  gastric  outline 
luminous  when  the  examination  is  made  in  a  dark  room.  The  most 
satisfactory  results  from  gastrodiaphany  have  been  secured  in  cases 
of  dilatation  and  prolapse,  but,  on  the  whole,  the  method  is  less 
dependable  than  examination  after  inflation  of  the  stomach  or.  by 
means  of  the  #-ray. 

Palpation. — Palpation  of  the  stomach  corroborates  the  findings 
of  inspection,  and  in  addition  reveals  and  localizes  gastric  pain  and 
tenderness,  tumors  and  thickening  of  the  anterior  wall,  and  suc- 
cussion  waves  within  the  organ;  exceptionally,  the  friction  fremitus 
of  a  perigastritis  can  also  be  felt.  In  studying  gastric  pain  it  is  help- 


526  PHYSICAL    DIAGNOSIS 

ful  to  recall  Riedel's  law,  that  left-sided  pain  generally  is  due  to 
disease  of  the  stomach  itself,  while  right-sided  pain  is  more  often  a 
reflex  sign  referable  to  lesions  of  other  abdominal  viscera,  the  princi- 
pal exceptions  to  this  general  rule  being  in  lesions  of  the  pan- 
creas and  of  the  pylorus. 

The  pain  of  gastritis  is  more  or  less  diffusely  distributed,  is  usually 
increased  by  pressure  and  by  taking  food,  and  intermits  without 
obvious  reason.  In  uncomplicated  gastralgia  the  pain  occurs  in 
neuralgic  paroxysms  which  commonly  radiate  peripherally  from  a 
point  low  down  in  the  epigastrium  and  are  relieved  both  by  pressure 
and  by  the  taking  of  food.  The  pain  of  gastric  ulcer  is  likely  to  be 
boring  and  scalding  in  character,  sharply  circumscribed  to  the  situa- 
tion of  the  lesion,  greatly  aggravated  by  taking  food  and  by  pressure 
and  relieved  by  vomiting;  a  tender  point  to  the  left  of  the  spine,  be- 
tween the  tenth  and  twelfth  thoracic  vertebrae,  is  of  considerable 
diagnostic  importance  (Fig.  68,  p.  1 19)  •  In  gastric  cancer  there  is  usu- 
ally a  dull,  gnawing  area  of  pain  localized  at  the  site  of  the  growth, 
reflected  toward  the  loins  and  the  back,  and  accompanied  by  tender- 
ness along  the  six  lower  thoracic  vertebrae;  the  pain  of  cancer  is  sub- 
ject to  frequent  periods  of  quiescence  and  to  paroxysmal  exacerba- 
tions of  a  gastralgic  form.  Other  important  gastric  factors  of  pain 
in  the  region  of  the  stomach  include  simple  irritation  of  the  organ, 
atonic  dyspepsia,  hyperchlorhydria,  gastrectasis,  and  gastroptosis. 
It  is  also  to  be  noted  that  pain  of  gastric  origin  may  be  simulated 
by  pneumonia,  pleurisy,  pericarditis,  spinal  caries,  Addison's  disease, 
locomotor  ataxia,  and  inflammatory  lesions  of  neighboring  abdominal 
organs. 

Tumors  of  the  stomach  are  most  frequently  found  at  the  pylorus, 
either  at  its  normal  site  or  lower  down,  owing  to  the  associated  changes 
in  the  size  and  position  of  the  organ.  Such  tumors  are  generally 
carcinomatous,  the  pylorus  being  the  favorite  seat  of  this  type  of 
neoplasm,  and  may  be  either  freely  movable  or  firmly  anchored, 
depending  upon  the  extent  to  which  they  are  bound  down  by  adhesions. 
Neoplasms  of  the  greater  curvature  may  be  palpable  in  the  hypogas- 
trium  or  in  either  hypochondrium;  growths  of  the  anterior  wall  are 
made  more  prominent  and  those  of  the  posterior  wall  are  obscured 
when  the  stomach  is  distended.  Riegel  emphasizes  the  importance 
of  distinguishing  a  tumor  of  the  lesser  curvature  from  the  pancreas, 
which  in  the  subject  with  a  thin,  relaxed  abdominal  wall  occasionally 
is  palpable  through  the  empty  stomach,  or  above  it,  if  the  organ  be 
displaced.  Inflation,  however,  will  settle  such  a  doubt  by  hiding 
the  pancreas  and  by  clearly  localizing  a  gastric  tumor.  Ewald  points 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     527 

out  that  in  various  forms  of  gastritis  the  inflammatory  swelling  of  a 
gastric  lymph-node  forms  a  small  movable  tumor  at  the  middle  of  the 
greater  curvature.  Hypertrophic  fibrosis  of  the  pylorus,  local  thick- 
ening of  the  anterior  wall,  nephroptosis,  fecal  masses,  and  small 
epigastric  hernias  are  other  abdominal  swellings  which  are  to  be  dis- 
tinguished from  tumors  of  the  stomach  itself. 

Succussion  sounds,  which  simply  mean  that  the  stomach  contains 
air  and  fluid,  are  elicited  bimanually,  with  one  hand  supporting  the 
subject's  flank  or  back  and  the  other  sharply  pushing  or  tapping  the 
abdomen  over  the  lower  gastric  area.  Since  identical  sounds  are  also 
produced  in  the  colon,  it  may  be  necessary,  in  the  doubtful  case,  to 
empty  either  the  stomach  or  the  gut  as  a  differential  procedure.  Gas- 
tric splashing  is  physiologic  when  detected  within  the  normal  bound- 
aries of  the  stomach  and  at  the  time  this  viscus  should  contain  food.  It 
is  pathologic  when  elicited  at  the  time  the  stomach  should  be  empty,  or 
when  it  occurs  well  beyond  the  normal  gastric  borders.  The  demon- 
stration of  succussion  splashing  three  or  four  hours  after  the  patient 
has  eaten  suggests  gastric  atony  or  motor  inadequacy;  and  the  pres- 
ence of  this  sign  outside  the  normal  limits  of  the  stomach  (especially 
below  the  navel)  is  strongly  indicative  of  the  organ's  enlargement 
or  dislocation. 

Here  may  be  mentioned  Stiller's  sign — undue  mobility  of  the 
tenth  rib — which  is  a  frequent  accompaniment  of  gastro-enteroptosis, 
with  or  without  gastric  atony  and  nervous  dyspepsia. 

The  Use  of  the  Stomach -tube. — This  instrument  is  employed 
in  securing  the  gastric  contents  for  analysis;  in  the  process  of  thera- 
peutic lavage;  in  rapidly  emptying  and  cleansing  the  stomach  and 
introducing  antidotes  in  poison  cases;  and  as  a  substitute  for  the 
esophageal  bougie  in  exploring  the  gullet.  Under  the  first-named 
circumstance  the  gastric  contents  should  be  withdrawn  by  passing 
the  tube  upon  the  expiration  of  a  definite  interval  after  the  patient 
has  eaten  a  standard  test-meal — one  hour  after  the  "roll  and  tea 
breakfast " 1  of  Ewald-Boas,  or  four  hours  after  the  test-meal 
of  Riegel.2  The  specimen  withdrawn  at  this  time  is  measured, 
inspected  for  naked-eye  changes,  tested  chemically,  and  exam- 
ined microscopically.  The  technic  of  these  procedures,  which  is  not 
germane  to  the  plan  of  this  work,  may  be  found  in  text-books  on  Clin- 
kal  Laboratory  Methods. 

1  One  dry  roll  (40  gm.)  and  a  cup  (400  cc.)  of  clear  tea. 

2  One  dry  roll  (40   gm.),  boiled  lean  meat  (200  gm.),  one  plate  of  gruel 
soup  (400  cc.),  and  one  glass  of  water  (200  cc.). 


528  PHYSICAL   DIAGNOSIS 

The  stomach- tube,  made  of  soft  rubber,  measures  about  3  feet 
(90  cm.)  in  length  and  J  inch  (8  mm.)  in  diameter,  having  at  the 
lower  extremity  a  double  fenestration  and  at  the  upper  a  funneled 
expansion;  a  circle  of  white  rubber  inlaid  at  a  point  22  inches 
(55  cm.)  from  the  gastric  end  of  the  tube  should  be  flush  with  the 
subject's  incisor  teeth  when  the  instrument  is  introduced  far  enough 
to  reach  the  stomach.  Before  using  it  is  well  to  warm  the  tube  by 
placing  it  in  hot  water,  and  to  lubricate  its  tip  by  smearing  it  with  a 
few  drops  of  glycerin.  When  there  is  reason  to  anticipate  obstinate 
choking  or  other  interference  with  the  introduction  of  the  tube,  pre- 
liminary spraying  of  the  posterior  pharynx  with  a  2  per  cent,  eucain 
solution  is  a  useful  preventive  step.  The  patient,  seated  with  the 
head  bent  forward,  the  mouth  open,  and  the  tongue  unprotruded,  is 
instructed  to  breathe  deeply  and  regularly,  whereupon  the  tube  is 
quickly  slipped  backward  along  the  posterior  pharynx  and  down 
into  the  esophagus,  at  the  entrance  to  which  a  muscular  contraction 
usually  arrests  the  instrument.  This  obstruction  is  but  temporary, 
however,  and  may  be  overcome  without  much  difficulty  by  making 
the  patient  swallow  and  take  very  deep  breaths;  when  freed,  the  tube 
is  quickly  pushed  down  until  it  has  entered  the  stomach.  The  patient 
now  bends  forward  and  strains  as  in  defecation  or  retches  as  in  vomit- 
ing, with  the  result  that  the  stomach  contents  begin  to  trickle  from 
the  funnel  end  of  the  tube,  which  should  drain  into  a  perfectly  clean 
receptacle.  A  sluggish  flow  may  be  overcome  by  "milking"  the  tube 
or,  preferably,  by  aspirating  into  a  Potain  vacuum  bottle.  Tubes 
equipped  with  a  bulb  should  not  be  used,  for  sanitary  reasons. 
After  the  stomach  has  been  thus  emptied  lavage  is  to  be  given,  by 
pouring  in  and  siphoning  out  sterile  water,  until  the  washings  return 
clear. 

Having  finished  the  above  procedures,  the  tube  is  removed  by  a 
continuous  sweep  of  the  examiner's  arm,  the  head  of  the  patient  mean- 
while being  turned  slightly  in  the  opposite  direction. 

The  use  of  the  stomach-tube  is  absolutely  interdicted  in  angina 
pectoris,  thoracic  aneurism,  advanced  cardiovascular  disease,  and 
recent  hemorrhage  from  any  source,  since  in  any  of  these  conditions 
the  stress  of  the  operation  may  be  perilous;  it  is  to  be  used  most 
cautiously,  if  at  all,  in  the  pregnant  woman,  in  markedly  cachectic 
and  enfeebled  persons,  and  in  those  suffering  from  active  broncho- 
pulmonary  lesions.  A  suspicion  of  esophageal  diverticulum  or  of 
ulcer  or  cancer  of  the  gullet  or  stomach  calls  for  great  care  in  tubing 
the  patient,  for  fear  of  mechanically  injuring  the  parts. 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     529 

Percussion. — To  map  out  by  percussion  the  tympanitic  area  of 
an  empty  normal  stomach  is  out  of  the  question,  since  in  this  state 
the  organ  recedes  beneath  the  left  dome  of  the  diaphragm.  This 
being  the  case,  the  zone  of  tympany  directly  below  the  liver  must  be 
due  to  the  transverse  colon,  which  rises  into  the  space  created  beneath 
the  anterior  abdominal  wall  by  the  recession  of  the  contracted  stomach. 


Hepatic  flatness 
Pulmonary  margin 

Traube's  semilunar 
space 

Lower  gastric 
border 


Fig.  208. — Percussion  area  of  gastric  tympany. 

Nor  can  the  lower  border  of  the  undistended  stomach  be  accurately 
delimited  by  percussion,  owing  to  its  curving  backward  away  from 
the  abdominal  parietes. 

In  the  moderately  distended  stomach,  however,  a  fairly  accurate 
region  of  pure  gastric  tympany  can  be  plotted  out  by  the  trained 
examiner.     The  following  boundaries  refer  to  the  tympanitic  region 
34 


53°  PHYSICAL    DIAGNOSIS 

delimited  with  the  subject  in  the  dorsal  decubitus:  upper  border, 
fifth  interspace  in  the  left  parasternal  and  midclavicular  lines;  lower 
border,  2  or  3  inches  (5  to  7.5  cm.)  above  the  umbilicus  in  the  median 
line  and  ninth  costal  cartilage  at  the  left  costal  margin;  right  border, 
2  inches  (5  cm.)  to  the  right  of  the  median  line;  and  left  border, 
seventh  interspace  in  the  left  anterior  axillary  line.  These  bound- 
aries are  necessarily  only  approximate,  owing  to  the  wide  variations 
in  the  size,  mobility,  and  distensibility  of  the  stomach  in  different 
individuals. 

Traube's  semUunar  space,  normally  affording  pure  gastric  tympany, 
corresponds  to  that  part  of  the  anterior  wall  of  the  stomach  lying 
directly  beneath  the  costal  parietes  (Fig.  208).  It  is  bounded  above 
by  the  left  lobe  of  the  liver  and  the  lower  border  of  the  left  lung; 
below  and  internally,  by  the  left  costal  margin;  and  externally,  by 
the  anterior  border  of  the  spleen.  The  tympany  of  this  area  is 
encroached  upon  by  flatness  from  above  in  left  pleural  effusion, 
massive  pericardial  effusion,  and  great  enlargement  of  the  heart, 
and  the  right  and  left  lateral  boundaries  are  similarly  affected  by 
enlargement  of  the  liver  and  of  the  spleen.  Extensive  left  basal 
pneumonia  impairs,  and  left  pneumothorax  apparently  extends,  the 
upper  (pulmonary)  limit  of  Traube's  space. 

In  delimiting  the  upper  border  percussion  should  be  continued 
from  below  upward  until  alterations  in  the  tympany  indicate  the 
margins  of  the  lung,  the  liver,  and  the  spleen;  the  deep-seated  fundus 
of  the  stomach  may  yield  a  muffled  tympany,  but  only  exceptionally 
is  it  recognizable  by  ordinary  percussion  methods.  To  facilitate 
mapping  out  the  lower  border,  the  patient,  standing  erect,  is  in- 
structed to  swallow,  in  several  tumblerful  draughts,  about  a  quart 
of  water,  with  the  result  that  a  flat  zone,  corresponding  to  the 
lowest  part  of  the  organ,  will  be  produced  by  the  ingested 
fluid.  This  flatness  increases  vertically  as  the  subject  swallows 
additional  fluid,  it  decreases  after  the  stomach  is  emptied  with 
the  stomach-tube,  and  it  shifts  or  disappears  as  the  patient 
changes  posture.  This  hydrostatic  test  is  essential  in  distinguishing 
gastric  and  intestinal  tympany  when  each  viscus  contains  air,  for 
unless  their  contents  differ  (i.  e.,  unless  one  contains  air  and  the  other 
liquid  or  solid  matter)  their  percussion  notes  are  so  similar  as  to 
defy  differentiation. 

In  practising  auscultatory  percussion  of  the  stomach  the  chest-piece 
of  a  binaural  stethoscope  is  placed  at  or  near  the  site  of  the  pylorus, 
and  light  percussion  begun  at  several  points  well  beyond  the  limits 


EXAMINATION   OF   ABDOMEN   AND   ABDOMINAL  VISCERA     531 

of  the  stomach  and  continued  toward  the  viscus,  which  when  reached 
is  betrayed  by  a  higher  pitched,  more  intense,  and  purer  note.  A  line 
connecting  the  points  at  which  these  changes  of  note  occur  obviously 
corresponds  to  the  outline  of  the  organ.  The  auscultatory  percussion 
tone  over  a  tumor  of  the  anterior  wall  of  the  stomach  sounds  much 
less  resonant  and  less  intense  than  the  note  elicited  over  the  healthy 
part  of  the  organ. 

Stroke  auscultation,  which  substitutes  a  gentle  stroking  of  the 
surface  with  the  finger  tips  for  actual  percussion,  is  employed  for  the 
same  purposes  as  auscultatory  percussion,  to  which  it  is  decidedly 
inferior  as  a  method  of  research. 

Increase  of  Gastric  Tympany. — Enlargement  of  the  area  of  gastric 
tympany  may  be  symptomatic  of  gaseous  distention,  pathologic 
dilatation,  or  dislocation  of  the  stomach,  and  in  all  of  these  conditions 
the  increase  is  chiefly  in  a  downward  direction.  A  horizontal  exten- 
sion of  tympany,  especially  of  the  right  border,  means  dilatation  of 
the  pyloric  region  with  deficient  motor  power  (Michaelis).  Several 
extrinsic  factors  of  increased  gastric  tympany  are  also  to  be  recalled — 
wasting  of  the  anterior  abdominal  parietes,  contraction  of  the  left 
lobe  of  the  liver,  retraction  and  emphysema  of  the  left  lung,  left 
pneumothorax,  and  perigastric  adhesions,  causing  downward  and 
forward  traction  of  the  stomach. 

Decrease  of  Gastric  Tympany. — The  area  of  epigastric  tympany 
is  symmetrically  contracted  when  actual  atrophy  of  the  stomach 
exists,  as  in  cirrhosis  ventriculi  and  in  cancer  or  other  stenotic  lesions 
of  the  cardia.  The  restriction  tympany  in  Traube's  semilunar  space 
has  been  alluded  to  in  a  preceding  paragraph. 

Auscultation.— The  deglutition  murmur  is  the  most  important 
single  finding  afforded  by  this  seldom-used  method  of  examining  the 
stomach.  It  is  audible  over  the  cardia,  usually  as  a  double  sound, 
and  is  elicited  by  auscultating  while  the  patient  swallows  a  mouthful 
of  water.  Normally,  the  primary  murmur  (esophageal)  is  heard 
about  six  seconds  after  the  act  of  deglutition,  and  the  secondary 
(gastric)  sound,  some  four  or  five  seconds  later.  The  absence  of 
these  two  murmurs  has  been  noted  in  stenosis  of  the  gullet  and  in 
enfeeblement  of  the  muscularis  of  this  tube.  Brenner  describes  a 
metallic  rub  audible  in  the  region  of  the  diaphragm  in  cases  of  per- 
foration of  the  stomach. 

Other  sounds  audible  over  the  gastric  area  include  succussion 
sounds  (described  above),  gurgling  arising  within  a  dilated  or  dis- 
placed stomach,  effervescence  of  fermenting  gastric  contents,  reso- 


532  PHYSICAL    DIAGNOSIS 

nant  echoes  of  the  heart  sounds  and  of  bronchopulmonary  rales, 
and  breath  sounds  transmitted  and  amplified  by  a  tensely  distended 
stomach. 

EXAMINATION  OF  THE  INTESTINES 

Clinical  Anatomy. — The  intestinal  canal  consists  of  two  principal 
divisions,  small  and  large,  the  former  being  a  highly  convoluted  and 
compact  central  mass  of  gut,  and  the  latter  a  stretch  of  larger  caliber 
and  of  less  twisted  contour.  The  greater  part  of  the  intestines  is 
covered  by  the  great  omentum  which  hangs,  curtain-like,  from  the 
lower  gastric  curvature  to  the  lower  part  of  the  hypogastric  region. 

The  small  intestine,  some  22  to  24  feet  (6.6  to  7  m.)  long,  occupies 
chiefly  the  umbilical,  lumbar,  and  hypogastric  regions,  and  stretches 
from  the  pyloric  end  of  the  stomach  to  the  ileocecal  valve,  its  lumen 
gradually  diminishing  from  2  inches  (5  cm.)  in  diameter  at  the  first 
point  to  i  inch  (2.5  cm.)  at  the  second.  The  duodenum,  or  the 
first  10  inches  (25  cm.)  of  the  small  gut,  runs  a  C-shaped  course  from 
the  pylorus  to  the  jejunum,  and  lies  almost  entirely  to  the  right  of 
the  median  line  of  the  belly,  occupying  the  lower  epigastrium 
and  the  upper  umbilical  region.  The  first  (upper)  part  of  the 
duodenum  is  behind  the  eighth  right  costal  cartilage  just  to  the 
left  of  the  gall-bladder;  the  second  (descending)  part  courses  vertically 
from  the  gall-bladder  along  the  downward  projection  of  the  right 
midclavicular  line,  in  front  of  the  right  kidney,  to  the  level  of  the  third 
or  fourth  lumbar  vertebra;  the  third  (lower)  part  runs  obliquely 
upward  from  this  point  to  the  left  of  the  second  or  third  lumbar 
vertebra,  where  it  twists  forward  to  form  the  duodenojejunal  flexure 
whose  surface  marking  corresponds  to  a  point  i  inch  (2.5  cm.)  to 
the  left  of  the  linea  alba  in  Lhe  transpyloric  line.  Clinically,  it 
is  important  to  know  that  the  duodenum  encircles  the  head  of  the 
pancreas;  that  it  lies  in  close  relation  posteriorly  with  the  portal 
vein,  common  bile-duct,  right  kidney,  and  inferior  vena  cava, 
and  anteriorly  with  the  liver,  gall-bladder,  and  transverse  colon; 
that  it  is  comparatively  immobile,  being  securely  anchored  to 
the  posterior  abdominal  wall.  The  jejunum,  which  includes  the 
next  8  feet  (2.15  m.)  of  the  small  gut,  lies  chiefly  in  the  upper 
umbilical  area  and  in  the  neighboring  regions  to  the  left,  while  the 
ileum,  forming  the  terminal  12  feet  (3.6  m.)  of  the  tube,  lies  below 
and  to  the  right.  On  their  course  toward  the  pelvis  the  coils  of  the 
small  intestine  cover  the  ascending  and  descending  colon  and  occupy 
the  greater  portion  of  the  umbilical,  lumbar,  and  hypogastric  areas. 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     533 

The  small  gut  is  so  exceedingly  mobile  that  the  above  regional 
arrangement  must  necessarily  be  only  approximate. 

The  large  intestine,  which  is  approximately  5  feet  (1.8  m.)  in 
length,  bounds  the  small  gut  and  extends  from  the  ileocecal  valve 
to  the  anus,  its  three  mam  divisions  being  the  cecum,  the  colon, 
and  the  rectum.  The  cecum,  a  superficial  wide  cul-de-sac  of  the 
large  gut,  is  in  the  right  iliac  fossa  below  the  ileocecal  valve,  whose 


Fig.  209. — Surface  topography  of  the  large  intestine. 


location  corresponds  to  a  point  on  the  anterior  abdominal  wall 
i  inch  (2.5  cm.)  below  the  middle  of  a  line  from  the  anterior  supe- 
rior iliac  spine  to  the  navel.  The  vermiform  appendix  springs 
from  the  posterolateral  surface  of  the  cecum,  and  may  stretch 
some  3  or  4  inches  (7.5  to  10  cm.)  in  length  behind  the  ileum,  toward 
the  pelvic  brim,  or  back  of  the  ascending  colon  (Fig.  209^).  The 
orifice  of  the  appendix  (at  Clado's  point)  lies  about  i  inch  (2.5  cm.) 
below  the  ileocecal, valve.  (Cf.  p.  519-) 


534  PHYSICAL   DIAGNOSIS 

Of  the  three  parts  of  the  colon,  the  first  or  ascending  passes  upward 
from  the  cecum  to  the  under  surface  of  the  right  costal  arch,  where 
below  the  liver  it  bends  sharply  to  the  left  to  form  the  hepatic  flexure. 
From  this  point  the  transverse  portion,  more  or  less  in  the  form  of  a 
U-shaped  tube,  loops  across  the  umbilical  region  to  the  left  costal 
arch  beneath  which  it  twists  upward,  backward,  and  to  the 


Fig.  2090. — Radiograph  of  the  vermiform  appendix  and  part  of  the  large  intestine. 
(Plate  by  Dr.  W.  F.  Manges.) 

left  as  the  splenic  flexure,  below  the  spleen  and  behind  the  stomach, 
and  at  a  higher  level  than  that  of  the  hepatic  flexure.  The  descending 
portion  of  the  colon  runs  down  the  left  side  of  the  abdomen  from  the 
splenic  flexure  to  the  iliac  crest,  where,  as  the  sigmoid  flexure  (or 
iliac  and  pelvic  colon),  the  gut  extends  through  the  pelvis  to  the 
rectum,  which  it  joins  opposite  the  third  segment  of  the  sacrum. 

Inspection  and  Palpation. — The  technic  and  general  results  of 
these  methods  have  been  dealt  with  under  Examination  of  the  Ab- 
domen. (See  pp.  500,  501.)  Applied  to  lesions  of  the  bowel, 
combined  inspection  and  palpation  is  the  most  satisfactory  means 
of  detecting  obstruction,  dislocation,  and  circumscribed  dilatation 
of  the  intestines,  and  tumors,  malignant,  inflammatory,  or  fecal. 

X-ray  examination  of  the  large  intestine  gives  additional  in- 
formation of  value,  and  defines  with  great  clearness  the  patency 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL   VISCERA     535 

of  the  ileocecal  valve  and  the  state  of  the  colon  and  the  lower 
portions  of  the  large  bowel.  In  connection  with  serial  radiography 
following  the  ingestion  of  a  bismuth  meal  (see  p.  524),  one  or  two 
plates  are  exposed  after  the  rectal  injection  of  a  barium  clyster. 
Cole  recommends  for  this  purpose  3  ounces  (85  gm.)  of  barium 
sulphate  dissolved  in  50  ounces  (i|  liters)  of  warm  water;  or  about 
34  ounces  (i  liter)  of  warm  water  containing  5  parts  of  barium 
sulphate  and  12  parts  of  mucilage  of  acacia  may  be  used.  The 
enema  is  instilled  slowly  by  gravity  through  a  rectal  tube,  and 


Fig.  210. — Abdominal  distention  due  to  dilatation  of  the  small  intestine  (Jefferson 

Hospital). 

should  be  retained  by  the  patient  until  the  plates  have  been 
exposed. 

Intestinal  obstruction,  leading  to  meteorism  of  the  gut  above 
the  site  of  the  stricture,  causes  distention  of  the  abdomen  vary- 
ing in  appearance  according  to  the  part  of  the  bowel  implicated. 
The  general  statement  holds  true,  that  the  more  remote  from  the 
duodenum  the  seat  of  the  obstruction  the  greater  the  degree  of  dis- 
tention. In  stenosis  near  the  ileocecal  valve  (the  favorite  site  of  intus- 
susception) the  brunt  of  the  distention  falls  upon  the  small  intestine 
whose  coils  balloon  the  central  part  of  the  abdomen  (Fig.  210),  where, 
in  the  thin-bellied  subject,  they  are  visible  as  a  series  of  transverse 
parallel  ridges  showing  exaggerated  peristalsis  and  paroxysms  of 


536 


PHYSICAL   DIAGNOSIS 


tetanic  contraction — the  so-called  "organ  pipe"  arrangement  of  the 
intestinal  loops.     To  the  touch  the  latter  feel  stiff  and  rigid  one 

moment,  but  gaseous,  fluctuating,  or 
pultaceous  the  next,  when  the  spasm 
temporarily  ceases,  with  a  gurgling 
sound  as  the  tension  lessens.  At 
the  site  of  the  stricture,  in  the  right 
iliac  fossa,  an  elongated  cylindric 
tumor  sometimes  may  be  felt.  In 
stenosis  near  the  sigmoid  (where 
volvulus  is  so  prone  to  occur)  this 
portion  of  the  large  intestine  and 
the  descending  colon  become  dis- 
tended to  an  extraordinary  degree, 
usually  first  bulging  the  left  iliac 
and  hypogastric  regions,  but  event- 
ually distending  the  greater  part  of 
the  abdomen,  the  tympanitic  gut 
often  taking  the  form  of  a  huge 
inflated  crescent,  with  its  convexity 
toward  the  right  loin  and  its  con- 
cavity encircling  the  navel.  Disten- 
tion  of  other  portions  of  the  colon 
is  recognized  by  the  presence  of  a 
cylindric  swelling  corresponding  to 
the  superficial  course  of  this  part 
of  the  intestinal  tract.  In  localizing 
the  seat  of  a  stenosis  of  the  colon, 
percussion  (q.  v.)  may  be  of  assist- 
ance. Inflation  of  the  intestines 
with  air  and  their  distention  with 
water  also  are  of  value  as  a  means 
of  determining  the  site  of  an  intes- 
tinal obstruction.  If  6  quarts  of 
water  can  be  introduced  with  a  foun- 
tain syringe,  there  is  no  obstruction 
in  the  large  intestine;  if  less  than 

4   quarts  can  be  injected,  there   is   probably  obstruction   in  the 
large  intestine   (J.  Chalmers  Da  Costa). 

So-called  idiopathic  dilatation  of  the  colon  leads  to  enormous  dis- 
tention of  the  large  bowel,  especially  near  the  sigmoid  flexure,  whence 
the  dilatation  tends  to  spread  upward.  In  such  instances  there  is 
remarkable  abdominal  enlargement  with  universal  tympany  extend- 


Fig.  211. — Abdominal  distention 
due  to  dilatation  of  the  colon  (Jef- 
ferson Hospital). 


EXAMINATION   OF  ABDOMEN  AND  ABDOMINAL  VISCERA     537 

ing  so  high  as  to  obscure  the  areas  of  hepatic  and  splenic  dulness 
(Fig.  211). 

Coloptosis,  or  downward  displacement  of  the  colon,  implicates 
chiefly  the  transverse  portion,  the  abnormal  outlines  of  which  are  readily 
seen  after  the  gut  has  been  inflated  with  air.  Commonly  a  dislocated 
colon  sags  downward  as  a  V-shaped  tube,  whose  convexity  lies  well 
below  the  navel;  sometimes,  by  traction  on  the  splenic  and  hepatic 
flexures,  it  causes  stenosis  at  these  points,  and  consequently  may 
lead  to  obstruction  of  the  large  bowel.  Coloptosis  rarely  exists 
without  gastroptosis  and  is  often  a  part  of  the  universal  dislocation 
of  the  abdominal  viscera  in  Glenard's  disease.  Ptosis  of  the  small 
intestine  doubtless  can  take  place,  though  it  is  not  evidenced  by  any 
distinctive  physical  signs. 

Fecal  impaction,  which  is  frequently  found  in  the  colon,  forms  an 
elongated  and  freely  movable  gut-shaped  tumor,  either  of  stony 
hardness  or  of  mushy  consistence,  more  commonly  the  former.  Such 
a  mass,  should  it  persist  after  free  purgation,  must  be  differentiated 
from  malignant  disease  of  the  intestine  by  a  detailed  physical  exami- 
nation and  by  a  critical  analysis  of  the  accompanying  symptoms. 
During  the  course  of  enteric  fever  a  soft  sausage-shaped  mass  in  the 
right  iliac  fossa  may  betray  intestinal  hemorrhage,  concealed  by 
reason  of  a  paretic  ileum;  gurgling  in  this  situation  is  in  nowise  dis- 
tinctive of  typhoid — it  simply  means  fluid  and  gas  within  the  gut. 
Appendical  thickening  or  abscess  may  account  for  a  more  or  less  well- 
defined  tender  mass  near  McBurney's  point,  provided  that  palpation 
is  not  interfered  with  by  the  board-like  muscular  rigidity  of  an  as- 
sociated peritonitis. 

In  chronic  appendicitis  Bassler's  method  of  pinching  the  appendix 
at  a  point  midway  between  the  umbilicus  and  the  right  anterior 
superior  iliac  spine  causes  acute  tenderness.  It  is  performed  by 
passing  the  tip  of  the  thumb,  held  vertically  and  pointing  toward 
the  ensiform,  into  the  abdominal  wall  at  the  point  indicated,  and 
then  swinging  it  to  the  right  so  as  to  pinch  the  appendix  against  the 
iliacus  muscle  and  thus  to  produce  sharp  pain.  Exquisite  tender- 
ness and  pain  is  produced  at  McBurney's  point  in  chronic  appendi- 
citis by  distending  the  colon  with  air  by  means  of  a  rectal  tube  and 
pump  (Bastedo's  sign). 

Pericolitis  sinistra,  an  inflammation  of  the  lower  part  of  the  descend- 
ing colon,  surrounding  connective  tissue,  and  peritoneum,  is  com- 
parable clinically  to  appendicitis,  except  for  its  situation  in  the  lower 
left  abdomen.  In  typical  cases  palpation  reveals  tenderness,  great 
muscular  rigidity,  and  an  elongated  tumor  in  the  sigmoid  region,  the 
associated  symptoms  pointing  to  local  peritonitis,  circumscribed 


PHYSICAL   DIAGNOSIS 

abscess,  or  general  peritonitis.  Obstinate  constipation  and  acquired 
diverticula  of  the  colon  are  the  two  most  common  underlying  causes 
of  this  type  of  colonic  inflammation. 

Malignant  disease  is  especially  prone  to  implicate  the  rectum,  the 
large  bowel  at  or  near  the  sigmoid,  hepatic,  or  splenic  flexures,  and  the 
duodenum.  When  it  invades  a  portion  within  reach  of  palpation  a 
roughly  spherical  or  ovoid  tumor  is  felt,  whose  consistence  is  generally 
hard  and  resistant,  and  whose  shape  is  unalterable  by  manipulation, 
differing  in  this  particular  from  a  fecal  tumor,  which  sometimes  can  be 
pitted,  dented,  and  otherwise  molded  by  firmly  pressing  it  between  the 
fingers.  The  mobility  of  the  tumor  depends  upon  its  situation  and 
upon  the  firmness  with  which  it  is  anchored  by  inflammatory  adhe- 
sions. Speaking  broadly,  cancer  of  the  sigmoid  and  of  the  cecum  are 
fixed,  while  cancer  of  the  small  intestine  is  relatively  movable.  When 
obstruction  exists  above  the  growth,  as  eventually  is  the  case  sooner 
or  later,  a  circumscribed  dilatation  of  the  gut  occurs  directly  above 
the  stricture;  this  pocket,  alternately  distending  with  feces  and  col- 
lapsing when  its  contents  are  expelled,  is  responsible  for  puzzling 
changes  in  the  size  and  the  shape  of  the  tumor,  which  even  may  quite 
disappear  for  days  at  a  time.  In  cancer  of  the  rectum  visual  exami- 
nation with  the  proctoscope  plus  digital  exploration  may  explain  the 
reason  for  the  unbearable  sacral  pain  and  acute  tenesmus  from  which 
the  patient  suffers. 

Aside  from  the  presence  of  a  circumscribed  tumor,  most  cases  of 
malignant  disease  of  the  bowel  are  attended  by  symptoms  of  ob- 
struction and  by  emaciation  and  cachexia.  In  perhaps  the  majority 
of  instances  enlargement  of  the  mesenteric  glands  and  of  the  superficial 
lymphatics  corroborates  the  other  findings. 

Percussion. — Percussion  of  the  intestines  is  useful  chiefly  in  con- 
firming the  findings  of  palpation,  in  conditions  such  as  those  just 
mentioned. 

Percussion  over  the  empty  colon  elicits  a  tympanitic  note  of  higher 
pitch,  somewhat  less  volume,  and  shorter  duration  than  is  found  over 
the  stomach.  The  note  over  the  small  intestine  is  also  tympanitic, 
and  of  still  higher  pitch,  less  volume,  and  less  drum-like  quality.  By 
ordinary  percussion  these  acoustic  differences  are  not  sufficiently 
marked  to  serve  as  reliable  criteria  in  mapping  out  the  different  parts 
of  the  gastro-intestinal  tract,  but  they  are  appreciable  by  ausculta- 
tory  percussion  or,  perhaps  better,  by  ordinary  percussion  after  dis- 
tention  of  the  colon  with  air.  This  is  accomplished  by  rectal  inflation 
with  a  Davidson  syringe,  after  having  emptied  the  large  bowel  by  an 
enema.  Ziemssen's  method  of  ballooning  the  colon  with  carbonic  acid 
gas  is  scarcely  to  be  advised  as  a  routine  procedure.  The  presence 


EXAMINATION  OF  ABDOMEN  AND   ABDOMINAL  VISCERA     539 

of  feces  within  the  intestines,  of  course,  modifies  the  above  findings; 
especially  in  the  right  iliac  region  and  left  flank  is  the  sound  likely  to  be 
dull,  since  it  is  in  the  cecum  and  sigmoid  that  fecal  matter  tends  to 
accumulate.  Impacted  feces  in  the  hepatic  and  splenic  flexures  may 
account  for  undue  extension  of  the  hepatic,  splenic,  and  renal  areas 
of  flatness. 

In  intestinal  obstruction  percussion  of  the  upper  lumbar  regions  is 
of  service  in  localizing  the  seat  of  the  stenosis.  A  loud,  deep  percus- 
sion sound  (dull  tympany)  is  found  here  on  both  sides  of  the  spine  in 
stenosis  of  the  descending  colon  and  sigmoid,  and  on  the  right  side 
only  in  stenosis  of  the  transverse  colon  and  splenic  flexure  (Noth- 
nagel) . 

Auscultation. — Auscultation  of  the  intestines  is  seldom  employed, 
except  in  connection  with  percussion,  to  delimit  different  segments 
of  the  intestinal  canal  and  to  detect  solid  tumors  thereof.  Like 
the  stomach,  the  intestines  afford  various  splashing,  gurgling,  and 
hissing  sounds  generated  by  the  movements  of  fluid  and  gas,  and, 
according  to  Sahli,  a  somewhat  distinctive  sizzling  or  whistling  noise 
is  occasionally  heard  over  an  intestinal  stricture  through  which 
gas  and  fluid  may  be  forced  by  peristalsis,  so  as  to  give  rise  to  audible 
and  perhaps  to  palpable  vibrations.  The  presence  of  a  distinct 
splashing  sound  just  above  the  point  of  obstruction  is  significant  of 
ileus. 

EXAMINATION  OF  THE  LIVER  AND  GALL-BLADDER 

Clinical  Anatomy. — Topographically,  the  liver  is  comparable 
to  a  wedge  driven  from  right  to  left  across  the  upper  zone  of  the 
abdomen  directly  beneath  the  diaphragm,  quite  three-fourths  of  the 
organ's  bulk  lying  to  the  right  of  the  median  line  of  the  trunk.  In 
the  adult  the  base  of  the  hepatic  wedge  occupies  the  right  hypo- 
chondrium,  the  middle  portion  fills  the  upper  epigastrium,  and  the 
sharp  convexity  tapers  off  into  the  left  hypochondrium  and  pro- 
jects some  2  or  2\  inches  (5  to  6.25  cm.)  beyond  the  left  sternal 
border  in  the  fifth  intercostal  space.  In  the  young  child  the  liver, 
being  disproportionately  large,  extends  well  beyond  the  limits  of 
the  right  hypochondrium,  and  encroaches  to  the  left  almost  as  far 
as  the  spleen.  The  falciform  ligament  and  the  longitudinal  fissure 
together  divide  the  liver  into  two  principal  lobes,  right  and  left, 
whose  point  of  divergence  at  the  inferior  parietal  aspect  of  the  organ 
anteriorly  is  indicated  by  the  umbilical  notch.  This  interlobar 
indentation  is  situated  in  the  epigastric  region  about  i  inch 
(2.5  cm.)  to  the  right  of  the  median  line,  at  the  level  of  the  ninth 
rib.  Just  below  and  external  to  this  point  lies  the  gall-bladder, 


540 


PHYSICAL   DIAGNOSIS 


whose  surface  marking  corresponds  to  the  angle  between  the  ninth  costal 
cartilage  and  the  external  border  of  the  right  rectus  abdominis  muscle. 
This  pear-shaped  structure,  approximately  3  inches  (7.5  cm.)  in 
length,  usually  reaches  to,  if  not  beyond,  the  lower  border  of  the 
liver,  but  its  exact  situation  is  subject  to  considerable  variation,  especi- 
ally in  a  horizontal  direction,  owing  to  individual  peculiarities  and 
to  the  mobility  of  the  liver,  with  which  it  must  move.  The  upper 
convex  surface  of  the  liver  lies  beneath  the  vault  of  the  diaphragm, 
and  is  anchored  to  this  muscle  and  to  the  anterior  abdominal  wall  by 
the  falciform  ligament,  a  peritoneal  reflection  springing  from  the 
upper  hepatic  border.  The  lower  concave  surface,  grooved  antero- 
posteriorly  by  the  longitudinal  fissure,  is  in  relation  with  the  stomach, 

the  hepatic  flexure  of  the  colon, 
and  the  right  kidney.  The 
anterior  surface,  thinning  out 
into  a  sharp  edge  behind  the 
right  costal  margin,  and  in- 
dented at  its  lower  border  by 
the  umbilical  notch,  lies  in 
contact  with  the  anterior  ab- 
dominal wall  for  a  distance 
of  2  or  3  inches  (5  to  7.5 
cm.)  below  the  base  of  the 
ensiform  cartilage.  The  right 
lateral  and  posterior  surfaces 
are  in  relation  with  the  abdom- 
inal wall  and  the  diaphragm, 
which  separates  the  liver  from 
the  inner  costal  surfaces  and 
the  lower  pulmonary  edges, 
while  behind  the  surface  bears 
the  impress  of  three  inti- 
mately related  structures:  an 
esophageal  groove,  a  vena 
caval  fossa,  and  a  right  supra- 
renal impression. 

The  surface  topography  of 
the  liver  is  represented  upon 
the  anterior  and  posterior  walls  of  the  thorax  by  a  wedge-shaped 
area,  having  its  apex  in  the  left  midhypochondrium  and  its  base 
directed  toward  the  right;  laterally,  the  outline  of  the  organ  is  irreg- 
ularly ovoid.  (Fig.  212;  also  Fig.  73,  p.  125.)  The  upper  border 


Fig.  212. — Surface   topography  of  the  liver 
and  gall-bladder. 


EXAMINATION  OP  ABDOMEN  AND  ABDOMINAL  VISCERA     541 

is  indicated  by  a  line  beginning  at  the  upper  part  of  the  fifth  left 
intercostal  space,  somewhat  internal  to  the  midclavicular  line,  and 
thence  encircling  the  right  half  of  the  chest  at  the  following  levels: 
sixth  chondrosternal  articulation  at  the  sternum,  fourth  interspace 
in  the  midclavicular  line,  seventh  interspace  in  the  midaxillary  line, 
eighth  rib  or  interspace  in  the  scapular  line,  and  eighth  thoracic 
vertebra  at  the  spine.  The  lower  border  passes  obliquely  downward 
and  toward  the  right  from  the  left  extremity  of  the  upper  level,  crosses 
the  left  costal  margin  at  the  eighth  costal  cartilage,  cuts  the  median 
line  about  midway  between  the  xiphisternal  joint  and  the  navel 
(in  the  transpyloric  line),  and  reaches  the  right  costal  margin  in 
the  right  Poupart  (midclavicular)  line;  thence  the  lower  level  dips 
below  the  tip  of  the  tenth  costal  cartilage,  and  passes  backward  to 
bridge  the  tenth  interspace  in  the  midaxillary  line  and  to  terminate 
alongside  the  spine  at  the  level  of  the  eleventh  thoracic  vertebra.  The 


Fig.  213. — The  hepatic  facies  (Jefferson  Hospital). 

upper  part  of  the  external  surface  of  the  liver  is  covered  by  the 
inferior  edge  of  the  right  lung  as  far  down  as  the  sixth  rib  in  the  mid- 
clavicular  line,  the  eighth  rib  in  the  midaxillary  line,  and  the  tenth 
rib  in  the  scapular  line. 


542  PHYSICAL    DIAGNOSIS 

Inspection. — In  examining  the  liver,  inspection  is  of  secondary 
importance  to  palpation  and  percussion.  A  greatly  enlarged  liver 
may  be  shown  by  bulging  of  the  lower  ribs  in  the  right  hypochondrium 
and  by  fulness  in  the  epigastrium  below  the  right  costal  margin,  but 
only  exceptionally  are  local  tumors  of  the  organ  recognizable  by 
inspection.  The  transmitted  impact  of  a  hypertrophied  heart  may 
be  forcible  enough  to  jar  the  liver  visibly,  and,  rarely,  pulsations  of 
the  liver  and  of  enlarged  superficial  veins  are  seen  in  conditions  of 
marked  venous  stasis.  Here  also  may  be  noted  the  peculiar  right- 
sided  sagging  of  the  trunk  of  the  patient  ill  of  hypertrophic  cirrhosis. 

The  hepatic  jacies  (Fig.  213)  of  the  subject  of  chronic  affections 
of  the  liver  is  characterized  by  a  muddy,  sallow  complexion  with 
more  or  less  anemic  pallor,  or  perhaps  by  the  typical  saffron  discolora- 
tion of  jaundice.  The  conjunctiva  are  similarly  tinged,  the  eyes  are 
watery  and  glistening,  and  beneath  the  skin,  which  is  commonly 
wrinkled  and  dry,  numerous  distended  venules  may  be  visible,  espe- 
cially about  the  nose. 

Radiographs  may  reveal  the  presence  of  gall-stones  if  the  calculi 
are  composed  largely  of  calcium,  but  cholesterin  stones,  which  but 
feebly  absorb  Rontgen  rays,  seldom  show  upon  the  plate. 

Palpation. — Tactile  sense  decides  the  questions  of  hepatic  tender- 
ness, pulsation,  friction,  and  thrills,  detects  extension  downward  of 
the  lower  border  of  the  liver,  and  determines  the  consistence  and  the 
contour  of  its  anterior  and  lower  surfaces. 

Tenderness  and  often  spontaneous  pain  in  the  hepatic  region  are 
common  symptoms  of  hepatic  congestion  and  of  various  inflammatory 
processes,  such  as,  for  example,  perihepatitis,  diffuse  hepatitis,  acute 
yellow  atrophy,  and  Hanoi's  cirrhosis.  Or  the  tenderness  may  be 
due  to  abscess,  cancer,  obstructive  jaundice,  or  fatty  degeneration. 
Hepatic  pain,  it  is  to  be  remembered,  is  not  always  localized,  but  may 
be  reflected  upward  to  the  right  shoulder  and  back  (Fig.  68,  p.  119). 
Gall-bladder  tenderness  is  commonly  referred  to  Robson's  point 
(q.  i).  5.).  In  many  inflammatory  conditions  of  the  liver  and  the 
gall-bladder  Bookman's  maneuver  is  useful  in  eliciting  acute  pain 
in  the  hepatic  area.  This  consists  of  forcing  the  umbilicus  down- 
ward toward  the  pubis  with  the  crooked  index-finger,  so  as  to  stretch 
the  round  ligament  and  consequently  to  exert  traction  upon  the 
liver  and  moderate  downward  and  forward  rotation  of  the  organ. 

Pulsations  of  the  liver  caused  by  the  thrust  of  a  hypertrophied 
heart  are  to  be  distinguished  from  those  due  to  congestion  of  the 
hepatic  venous  channels.  In  the  former  the  "jogging"  character  of 
the  impulse,  the  physical  signs  of  right  ventricular  hypertrophy,  and 
the  absence  of  tricuspid  leakage  are  the  cardinal  diagnostic  points; 


EXAMINATION  OF  ABDOMEN  AND  ABDOMINAL  VISCERA     543 

in  the  latter  the  expansile,  resilient  impulse,  the  murmur  of  tricuspid 
insufficiency,  and  pulsation  of  the  jugulars  form  a  characteristic 
trinity  of  signs.  Dynamic  throbbing  of  the  abdominal  aorta  also 
is  to  be  differentiated  from  hepatic  pulsation.  The  friction-rub 
of  perihepatitis  and  the  thrill  elicited  by  palpatory  percussion 
over  a  hydatid  cyst  have  been  described  elsewhere.  (See  pp.  135 
and  516.) 

With  complete  abdominal  relaxation,  enlargement  and  descent 
of  the  liver  are  readily  determined  by  palpatingx  the  upper  abdom- 
inal zone,  with  the  finger-tips  pointing  upward  toward  the  hepatic 
area;  or  the  bimanual  method  may  be  more  satisfactory  (Fig. 
214).  Except  in  the  young  child  and  in  the  wasted  adult,  it  is  not 


Fig.  214. — Bimanual  palpation  of  the  liver. 

always  possible  to  feel  the  sharp  lower  border  of  the  normal  liver 
below  the  right  costal  arch  and  in  the  epigastrium,  owing  to  the  re- 
sistance offered  by  the  abdominal  musculature  and  fat.  With  deep 
inspiration  an  enlarged  or  a  depressed  liver  is  felt  to  descend 
and  with  expiration  to  ascend,  this  respiratory  movement  being  a 
valuable  point  of  distinction  between  hepatic  enlargements  and  intra- 
abdominal  tumors  not  connected  with  the  liver,  and  hence  fixed  during 
respiration.  A  rigid  right  rectus  muscle  must  always  be  considered 
as  a  possible  counterfeit  of  a  neoplasm  of  the  right  lobe  of  the  liver. 
In  enlargements  of  the  liver  it  is  important  to  find  the  umbilical  notch, 
on  either  side  of  which  lie  the  right  and  the  left  lobes  (see  p.  539). 

In  the  presence  of  ascites  or  of  meteorism  it  may  be  impossible 
to  feel  the  lower  edge  of  the  liver,  although  it  extends  far  below 


544  PHYSICAL   DIAGNOSIS 

the  margin  of  the  ribs.  In  the  former  condition  "dipping"  (p.  501) 
should  be  tried  or  aspiration  may  be  necessary  to  drain  off  the 
interposed  fluid;  in  the  latter  the  liver  may  sometimes  be  felt 
by  Gtenard's  method — strong  pressure  with  the  fingers  of  the  left 
hand  upon  the  right  lumbar  region  and  palpation  with  the  left 
thumb  below  the  right  costal  margin,  meanwhile  exerting  deep 
rotary  pressure  with  the  right  hand  across  the  upper  abdomen,  the 
lumbar  pressure  forcing  the  liver  down  and  the  abdominal  pressure 
pushing  the  intestine  away  from  the  belly  wall  and  up  beneath  the 
liver,  so  that  it  may  be  felt  by  the  examiner's  thumb  (Fig.  215). 
The  consistence  and  the  contour  of  the  liver,  which  vary  greatly  in 


Fig.  215. — G16nard's  method  of  palpating  the  liver. 

different  pathologic  conditions,  are  sometimes  characteristic  of 
certain  lesions  causing  hepatic  enlargement.  The  consistence  of  the 
liver  may  be  dense,  yielding,  or  fluctuating;  its  surface,  smooth,  rough, 
or  nodular;  and  its  contour,  furrowed,  notched,  or  lobulated. 

In  amyloid  disease  the  texture  of  the  liver  feels  dense  and  unyield- 
ing, its  surface  is  uniformly  smooth  and  even,  and  its  lower  border  is 
blunt  and  rounded.  Increased  hardness  of  the  liver  may  also  result 
from  cirrhosis,  cancer,  syphilitic  hepatitis  or  capsulitis,  and  leukemic 


EXAMINATION   OF  ABDOMEN   AND  ABDOMINAL  VISCERA     545 

infiltration.  A  local  resilient,  perhaps  fluctuating,  area  elevated 
above  the  surface  of  the  organ,  suggests  circumscribed  abscess, 
hydatid  cyst,  or  gumma. 

The  contour  is  regular  and  the  surface  unroughened  in  the  amyloid, 
fatty,  cyanotic,  and  leukemic  livers;  in  diffuse  non-purulent  hepatitis 
and  in  generalized  abscess;  and  in  the  enlargements  associated  with 
febrile  states,  biliary  obstruction,  pseudoleukemic  anemia,  Banti's 
disease,  and  other  primary  anemias.  In  Hanot's  cirrhosis  the  surface 
of  the  liver  is  generally  smooth  or  but  little  roughened.  It  is  rough, 
nodular,  or  lobulated  in  atrophic  and  syphilitic  cirrhoses,  in  cancer, 
and  in  deformity  due  to  local  constriction.  In  so-called  corset-liver 
there  may  be  a  more  or  less  oval  projection  of  the  right  lobe  extend- 
ing downward  several  inches  below  the  infracostal  line,  or  in  the 
extreme  instance,  as  far  as  the  level  of  the  umbilicus.  A  slender 
tongue-like  extension  of  the  liver  below  the  right  costal  border 
{RiedeVs  lobe)  is  occasionally  appreciable  in  cholelithiasis  attended 
by  great  enlargement  of  the  gall-bladder. 

A  normal  gall-bladder,  unless  distended  with  bile,  is  not  palpable, 
but  when  enlarged  it  may  produce  a  circumscribed  globular  bulging 
just  below  the  right  costal  margin,  or  lower,  if  the  distention  be  suffi- 
cient greatly  to  elongate  the  organ,  the  dimensions  of  which  occa- 
sionally are  most  extraordinary.  Exceptionally,  the  gall-bladder 
enlarges  in  an  upward  direction  and  is,  therefore,  impalpable.  When 
filled  with  calculi,  a  crunching  gall-stone  crepitus  can  sometimes  be 
felt. 

Percussion. — By  percussion  one  is  able  to  decide,  by  mapping  out 
the  boundaries  of  the  hepatic  area,  whether  the  size  of  the  liver  is 
normal,  increased,  or  diminished,  and  whether  the  organ  is  displaced 
either  upward  or  downward.  Both  ordinary  and  auscultatory  per- 
cussion are  useful  in  the  examination  of  the  liver,  the  latter  method 
being  especially  adapted  to  the  localization  of  solid  tumors. 

The  vertical  surface  measurement  of  the  hepatic  area  is  about  4 
inches  (10  cm.)  in  the  median  and  midclavicular  lines,  6  inches 
(15  cm.)  in  the  midaxillary  line,  and  3  inches  (7.5  cm.)  in  the 
scapular  line.  These  figures,  which  refer  to  the  average  healthy 
adult,  are  somewhat  less  in  extreme  old  age  and  in  the  deep-chested 
subject;  in  the  young  child  the  surface  area  of  the  liver  is  relatively 
more  extensive  than  in  the  adult. 

The  Areas  of  Hepatic  Dulness  and  Flatness. — The  liver,  like  the 
heart,  presents  two  different  percussion  zones,  which  may  be  con- 
veniently designated  as  hepatic  dulness  and  as  hepatic  flatness 
(Fig.  216).  The  area  of  hepatic  dulness,  corresponding  to  that 
part  of  the  upper  right  lobe  separated  from  the  chest  wall  by 
35 


546 


PHYSICAL   DIAGNOSIS 


the  lower  pulmonary  margin,  affords,  on  forcible  percussion,  a 
dulness  tempered  by  the  resonant  quality  of  the  intervening  vesicular 
structure.  The  area  of  hepatic  flatness,  situated  below  the  preceding 
and  overlying  that  part  of  the  organ  directly  in  contact  with  the  inner 
costal  wall,  is  elicited  by  percussion  of  moderate  force,  and  yields 
no  trace  of  pulmonary  resonance,  the  sound  thereover  being  unquali- 
fiedly flat  and  high  pitched. 

To  determine  the  upper  limit  of  hepatic  dulness,  the  right  side  of 


Fig.  216. — Percussion  areas  of  hepatic  dulness  and  flatness. 

the  chest  is  percussed  from  above  downward,  beginning  at  a  level 
sufficiently  high  to  demonstrate,  for  the  sake  of  comparison,  pure 
vesicular  resonance.  Carrying  the  percussion  lines  vertically  down- 
ward from  the  second  or  third  interspace,  in  the  right  midclavicular 
line  the  pulmonary  resonance  becomes  modified  and  obviously  im- 
paired as  the  fourth  interspace  is  crossed;  in  the  midaxillary  line  this 
change  is  noted  at  the  seventh  interspace,  and  in  the  scapular 
line,  at  the  eighth  interspace.  Having  thus  delimited  the  upper 
border  of  the  hepatic  area,  percussion  is  continued  downward  along 
the  three  lines  just  indicated,  until  the  level  of  hepatic  flatness  is 
reached  at  the  sixth,  eighth,  and  tenth  ribs  in  the  midclavicular, 


EXAMINATION  OF  ABDOMEN  AND   ABDOMINAL' VISCERA     547 

midaxillary,  and  scapular  lines,  respectively.  The  dull  region 
bounded  by  the  horizontal  limits  thus  mapped  out  represents  the 
area  of  hepatic  dulness.  The  area  of  hepatic  flatness  extends  down- 
ward in  the  midclavicular  line  to  the  right  costal  margin,  in  the  mid- 
axillary  line  to  the  tenth  intercostal  space,  and  in  the  scapular  line 
it  cannot  be  distinguished  from  the  flatness  of  the  right  kidney  with 
which  it  is  continuous.  In  the  epigastrium  hepatic  flatness  extends 
downward  in  the  median  line  for  a  distance  of  about  3  inches  (7.5  cm.) 
below  the  xiphoid.  As  already  pointed  out,  it  is  impracticable  to  de- 
limit the  hepatic  and  cardiac  flatness  at  their  junction  near  the  sixth 
left  chondrosternal  articulation.  In  mapping  out  the  lower  border  of  the 
liver  anterolaterally,  two  fallacies  must  be  avoided:  the  predominant 
tympany  of  the  gut  and  stomach,  and  the  dull  overtone  arising  from 
the  abdominal  musculature.  To  minimize  these  two  sources  of  error, 
the  thin  lower  margin  of  the  liver  should  be  percussed  very  gently, 
so  that  the  flat  hepatic  sound  may  not  be  masked  by  loud  tympany 
on  the  one  hand,  or  be  blended  with  muscle  dulness  on  the  other. 

A  normal  gall-bladder  lies  beyond  the  reach  of  percussion,  but  when 
enlarged  it  affords  flatness  continuous  with  that  of  the  liver,  unless, 
as  sometimes  happens,  a  coil  of  gut  has  become  pushed  in  between 
the  two,  so  as  to  separate  them  by  a  transverse  band  of  tympany. 

Enlargement  of  the  liver  is  indicated  by  lengthening  of  the  vertical 
lines  of  the  hepatic  area  with  a  palpable  tumor  below  the  right  costal 
margin,  a  general  increase  in  the  hepatic  volume  being  met  with  in 
circulatory  disturbances  and  in  structural  lesions  of  the  organ,  in 
biliary  obstruction,  in  certain  of  the  primary  anemias,  and  in  various 
diseases  of  the  blood.  Thus,  the  liver  is  unnaturally  enlarged 
in  active  and  passive  congestion,  acute  hepatitis,  Hanoi's  cirrhosis, 
syphilis,  fatty  infiltration,  amyloid  disease,  abscess,  solid  tumors,  and 
cysts;  in  obstruction  of  the  bile-ducts  and  in  Weil's  disease;  and  in 
leukemia,  Banti's  disease,  kala-azar,  trypanosomiasis,  malarial  fever, 
enteric  fever,  and  relapsing  fever.  A  fictitious  enlargement  of  the 
liver  may  be  produced  by  the  basal  dulness  of  right  pleural  effusion 
or  of  extensive  croupous  pneumonia.  Subphrenic  abscess  may  have 
the  same  effect,  and,  should  an  anterior  intraperitoneal  abscess 
form,  there  may  be,  in  addition  to  increase  hi  the  hepatic  area  verti- 
cally, a  triangular  bulging,  fluctuating,  flat  area  lying,  base  down- 
ward, between  the  median  line,  the  lower  border  of  the  liver,  and 
the  left  costal  arch. 

Decrease  in  the  size  of  the  liver  accompanies  acute  yellow  atro- 
phy, as  well  as  advanced  Laennec's  cirrhosis,  in  which  condi- 
tions the  recession  of  the  organ  from  the  parietes  leaves  a  space 
filled  with  coils  of  gut  whose  loud  tympany  may  entirely  obliter- 


548  PHYSICAL    DIAGNOSIS 

ate  every  vestige  of  hepatic  flatness.  True  hepatic  atrophy 
must  be  carefully  distinguished  from  simulated  decrease  in  the 
size  of  the  liver  due  to  certain  intrathoracic  and  intra-abdominal 
factors:  the  upper  zone  of  the  hepatic  surface  area  may  be  de- 
cidedly encroached  upon  by  the  downward  extension  of  hyperreso- 
nance  in  emphysema  of  the  right  lung,  or  by  the  impingement  of  a 
pneumothoracic  right  pleural  sac;  and  the  lower  zone  may  be  similarly 
affected  by  a  mass  of  tympanitic  intestine  crowded  upward  between  the 
anterior  surface  of  the  liver  and  the  costal  parietes,  or  by  the  ascent 
of  free  gas  within  the  peritoneal  cavity. 

Enlargement  of  the  gall-bladder  may  be  symptomatic  of  local 
hydrops,  empyema,  calculi,  or  malignant  disease,  and  also  of  biliary 
obstruction  incident  to  simple  catarrhal  inflammation,  intestinal 
parasites,  and  the  pressure  of  enlarged  glands  or  neoplasms,  as  in 
cancer  of  the  head  of  the  pancreas  or  of  the  pylorus.  In  this  connec- 
tion one  should  recall  the  practical  application  of  Counwisier's  law, 
that  enlargement  of  the  gall-bladder  plus  jaundice  suggests  biliary 
obstruction  from  malignant  disease  rather  than  from  cholelithiasis 
of  other  causes. 

Displacement  of  the  liver  is  betrayed  by  unnatural  elevation  or 
depression  of  the  horizontal  hepatic  levels,  unattended  in  simple 
displacement  by  deviation  from  the  normal  vertical  measurements 
of  the  hepatic  area.  Upward  displacement  is  referable  chiefly  to 
extrahepatic  factors,  such  as  excessive  subphrenic  pressure,  intra- 
thoracic traction  and  pulmonary  collapse,  and  paralysis  of  the  dia- 
phragm. Thus,  the  liver  may  be  crowded  far  upward  by  the  pressure 
of  ascites,  meteorism,  or  abdominal  tumor;  pulled  upward  by  a  cir- 
rhosed,  atelectatic  right  lung;  or  pushed  to  an  unusually  high  level 
when  a  paralyzed  diaphragm  is  forced  upward  by  the  unopposed 
action  of  the  abdominal  muscles.  Downward  displacement,  which  is 
much  the  commoner,  is  generally  traceable  to  lesions  of  the  thorax, 
the  heart,  or  the  subphrenic  space;  less  commonly  to  diseases  of 
the  liver  itself.  An  emphysematous  lung,  a  right-sided  intra- 
pleural  neoplasm  or  effusion  of  air  or  of  fluid  may  exert  sufficient 
downward  pressure  upon  the  diaphragm  to  depress  the  liver  be- 
low the  costal  margin;  and,  in  extreme  cases,  a  cardiac  enlarge- 
ment can  have  the  same  effect.  The  liver  may  also  be  depressed 
by  the  weight  of  a  pus  accumulation  beneath  the  diaphragm — sub- 
phrenic  abscess.  Hepatoptosis,  or  prolapse  of  the  liver,  which  also 
drags  down  the  hepatic  surface  area,  may  exist  alone  or  in  associa- 
tion with  ptoses  of  other  organs,  as,  for  example,  of  the  stomach 
(gastroptosis) ,  of  the  intestines  (enteroptosis) ,  of  the  spleen  (splen- 
optosis) ,  and  of  the  kidneys  (nephroptosis) .  A  prolapsed  liver  forms 


EXAMINATION  OF   ABDOMEN  AND   ABDOMINAL  VISCERA     549 

a  rounded,  notched  mass  having  a  smooth  surface  in  the  upper 
abdominal  region,  the  tumor  being  easily  removed  by  bimanual 
manipulation,  and  showing  a  restricted  respiratory  rise  and  fall. 
Above  the  tumor,  in  the  lower  right  hypochondrium,  the  normal 
area  of  hepatic  flatness  is  replaced  by  intestinal  tympany. 

Auscultation. — As  applied  to  examination  of  the  liver  and  gall- 
bladder, auscultation  is  resorted  to  only  in  exceptional  instances,  and 
then  in  confirmation  of  signs  otherwise  obtained.  For  example, 
a  soft  rustling  perihepatitic  friction-sound  provoked  by  respiration 
is  sometimes  demonstrable  over  the  right  hypochondrium  when  the 
peritoneal  capsule  of  the  liver  is  the  seat  of  fibrinous  roughening. 
Gall-bladder  friction-sounds  and  gall-stone  crepitations  are  auscul- 
tatory  findings  occasionally  met  with  in  cholelithiasis,  and  in  gall- 
bladder distention  and  displacement  C.  M.  Cooper  has  noted  a  sys- 
tolic souffle  attributable  to  pressure  upon  the  epigastric  artery.  Caval 
compression  may  account  for  a  venous  bruit  audible  over  the  hepatic 
area,  while  cirrhosis  of  the  liver  is  sometimes  attended  by  venous  mur- 
murs heard  most  distinctly  just  below  the  ensiform,  and  due  to  dif- 
ferences in  pressure  within  the  epigastric  veins  and  tributaries  (Catti) . 

EXAMINATION  OF  THE  PANCREAS 

Clinical  Anatomy. — The  pancreas  is  an  elongated  structure 
about  6  inches  (15  cm.)  in  length,  shaped  somewhat  like  a  blunt 
hook,  and  lying  chiefly  in  the  epigastrium,  about  midway  between 
the  umbilicus  and  the  tip  of  the  xiphoid.  The  organ  stretches  trans- 
versely between  the  duodenum  on  the  right  and  the  spleen  on  the 
left,  and  corresponds  anatomically  to  the  level  of  the  first  and  second 
lumbar  vertebrae  (Fig.  217).  The  head  of  the  pancreas  is  enclosed 
by  the  concavity  of  the  duodenum,  and  lies  opposite  the  second 
lumbar  vertebra;  the  neck  coincides  with  the  junction  of  the  median 
line  of  the  abdomen  with  the  transpyloric  line,  just  above  and  to 
the  left  of  which  lies  the  body  ;  the  tail  extends  into  the  left  hypo- 
chondrium as  far  as  the  hilus  of  the  spleen.  Anteriorly  the  pancreas 
is  covered  by  the  stomach,  transverse  colon,  and  small  intestine; 
posteriorly  it  is  in  relation  with  the  common  bile-duct,  portal  vein, 
inferior  vena  cava,  aorta,  left  kidney,  and  spleen. 

Physical  Examination. — The  normal  pancreas,  being  so  deeply 
seated,  cannot  be  reached  through  the  abdominal  wall,  except  per- 
haps in  the  old,  emaciated  subject  and  in  one  whose  stomach  lies 
abnormally  low;  in  such  cases  the  organ  occasionally  is  palpable  as 
a  resistant  mass  horizontally  crossing  the  epigastrium.  An  area  of 
increased  resistance,  less  commonly  an  immobile  tumor,  in  the 


550 


PHYSICAL    DIAGNOSIS 


central  or  the  right  epigastric  region  may  be  felt  in  the  event  of  a 
pancreatic  enlargement,  due,  for  example,  to  acute  hemorrhage  and 
inflammation,  to  sclerosis,  or  to  a  new  growth.  But  only  when  these 
signs  are  accompanied  by  such  symptoms  as  violent  abdominal  pain, 
jaundice,  edema,  and  mydriasis  after  the  instillation  of  adrenalin, 


Duodenum 


Fig.  217.  —  Surface  topography  of  the  pancreas. 

and  by  such  laboratory  findings  as  fatty  stools  and  glycosuria,  is  the 
diagnosis  of  a  lesion  of  the  pancreas  justifiable. 


EXAMINATION  OF  THE   SPLEEN 

Clinical  Anatomy. — The  spleen  is  a  viscus  of  ovoid  shape,  situated 
in  the  left  hypochondrium,  with  its  long  axis  running  obliquely  down- 
ward and  forward  from  a  point  i£  inches  (3.75  cm.)  from  the  left  of 
the  tenth  thoracic  spine  to  the  tenth  rib  in  the  midaxilla  (Fig.  218). 
The  diaphragmatic  surface  is  convex,  and  lies  directly  beneath  the  in- 
ferior surface  of  the  diaphragm;  the  gastric  surface,  which  is  concave, 


EXAMINATION  OF  ABDOMEN  AND   ABDOMINAL  VISCERA     551 

borders  upon  the  fundus  of  the  stomach;  the  renal  surface,  or  the 
tapered  upper  and  posterior  extremity,  lies  in  close  contact  with  the 
left  kidney,  the  percussion  areas  of  the  two  organs  merging ;  and  the 
intestinal  surface,  notched  and  lying  anteriorly,  is  in  relation  with  the 
splenic  flexure  of  the  colon.  The  upper  one-third  of  the  spleen, 
being  covered  by  the  lung,  pleura,  and  diaphragm,  is  beyond  the  reach 
of  physical  examination,  but  its  lower  two-thirds,  lying  immediately 
against  the  chest  wall,  is  accessible. 

Inspection. — Save  in  examples  of  extreme  splenomegaly,  causing 
conspicuous  distention  of  the  splenic  area,  visual  examination  of  the 
spleen  is  of  no  service. 


Fig.  218. — Surface  topography  of  the  spleen. 

Palpation. — This,  by  far  the  most  useful  method  of  exploring 
the  spleen,  determines  the  important  questions  of  tenderness  and  of 
enlargement.  The  patient  should  lie  in  dorsal  decubitus  with  the 
abdomen  relaxed,  while  the  examiner,  standing  at  the  right  of  the 
bedside,  applies  the  palm  of  his  right  hand  to  the  belly  wall  and 
forcibly  pushes  upward  with  the  finger-tips  beneath  the  left  costal 
margin,  the  left  hand  meanwhile  firmly  raising  the  patient's  left 
loin,  so  as  to  elevate  the  spleen  (Fig.  219).  The  spleen  of  normal 


552 


PHYSICAL   DIAGNOSIS 


size  cannot  be  felt  beneath  the  costal  border,  but  if  it  be  even  mod- 
erately enlarged,  its  impingement  against  the  finger-tips  with  each 
inspiration  of  the  patient  and  its  recession  from  them  with  each  expi- 


Fig.  aiQ. — Bimanual  palpation  of  the  spleen. 

ration  is  clearly  appreciable;  if  decidedly  enlarged,  the  organ  is  recog- 
nized as  a  much  bulkier  tumor,  which  moves  diagonally  upward  and 


Fig.  220. — Compression-palpation  of  the  spleen. 

downward  with  respiration.  Grasping  the  patient's  left  flank  with 
forcible  compression  while  the  thumb  feels  for  the  organ,  also  is  an 
excellent  method  of  detecting  a  splenic  enlargement  (Fig.  220). 


EXAMINATION   OF   ABDOMEN    AND   ABDOMINAL   VISCERA 


553 


Tenderness  and  pain  in  the  region  of  the  spleen  are  met  with  in 
perisplenitis,  and  in  infarction,  abscess,  acute  congestion,  and 
other  forms  of  .enlargement  of  the  organ.  Signorelli's  spleen  point, 
to  which  cutaneous  pain  is  referred  in  inflammatory  lesions  of  the 
spleen,  is  situated  at  or  near  the  intersection  of  the  left  fifth  inter- 
space and  the  midclavicular  line.  Pulsation  of  the  spleen  has  been  de- 
scribed as  a  rare  finding  in  Corrigan's  disease. 

Enlargement  of  the  spleen,  of  rapid  development  and  moderate 
extent,  is  a  pertinent  physical  sign  in  various  acute  specific  infections, 
of  which  the  following  are  typical  examples:  malarial  fever,  relapsing 
fever,  sepsis,  typhoid  fever,  typhus 
fever,  acute  miliary  tuberculosis, 
tuberculous  peritonitis,  erysipelas, 
diphtheria,  variola,  scarlatina,  pneu- 
monia, epidemic  cerebrospinal  fever, 
acute  yellow  atrophy  of  the  liver, 
and  Weil's  disease.  In  trypano- 
somiasis  and  in  kala-azar  the  organ 
enlarges  progressively  and  some- 
times to  an  extraordinary  dimen- 
sion. Of  most  of  the  primary 
enemias  this  is  also  true — myelogen- 
ous  and  lymphatic  leukemia,  Banti's 
disease,  von  Jaksch's  anemia,  and 
pernicious  anemia.  Amyloid  dis- 
ease, Hanoi's  cirrhosis,  syphilis, 
rickets,  acromegaly,  Pick's  dis- 
ease, and  pancreatic  cirrhosis  serve 
to  illustrate  chronic  diseases  of 
which  moderate  splenic  enlarge- 
ment is  symptomatic,  and  to  these 
may  be  added  certain  lesions  induc- 
ing venous  congestion,  such  as  chronic  cardiac  disease,  hepatic  cir- 
rhosis, and  tumors  causing  pressure.  In  tumors  of  the  spleen,  such 
as  hydatid,  cancer,  or  lymphadenoma,  and  in  abscess  various  grades 
of  enlargement,  generally  of  irregular  contour,  are  encountered. 

Downward  displacement  of  the  normal  spleen,  simulating  actual 
enlargement,  may  be  the  result  of  lesions  of  the  left  thorax  that  exert 
pressure  upon  the  upper  surface  of  the  organ,  as  in  emphysema, 
pleural  effusion,  pneumothorax,  and  extensive  neoplasm.  Upward 
displacement  of  the  organ  is  a  change  secondary  to  meteorism  and 
ascites,  -and  to  a  contracted  left  lung  or  pleura.  The  differentiation 


Fig.  221. — Leukemic  enlargement  of 
the  spleen  (Jefferson  Hospital). 


554 


PHYSICAL   DIAGNOSIS 


of  splenic  displacement  and  enlargement  is  based  partly  upon  the 
detection  of  one  of  the  above-named  factors  of  ptosis  and  partly 
upon  the  delimitation  of  the  organ's  upper  border  by  percussion. 
In  splenoptosis  the  spleen  may  sag  downward  as  far  as  the  umbilicus 
or  even  into  the  pelvis,  while  in  the  axillary  region  of  normal  splenic 
dulness  the  note  is  tympanitic.  The  dislocated  organ,  provided  that 
its  migration  has  not  been  complicated  by  inflammatory  adhesions, 


Midaxillary  line 
Ninth  rib 
Pulmonary  border 
Splenic  dulness 
Eleventh  rib 


Fig.  222. — The  area  of  splenic  dulness. 

is  readily  palpable  as  a  freely  movable  mass,  of  smooth  lieniform 
contour,  of  which  the  oval  shape  and  notched  border  are  the  iden- 
tifying marks. 

Percussion. — The  patient  should  either  stand  erect  or  lie  partly 
upon  the  right  side  (right  diagonal  decubitus),  with  the  left  arm 
thrown  across  the  thorax  or  above  the  head.  Percussion  over  the 
anterior  and  inferior  borders  of  the  spleen  must  be  very  gentle,  in 


EXAMINATION   OF   ABDOMEN   AND   ABDOMINAL    VISCERA       555 

order  to  avoid  the  production  of  a  dominant  tympanitic  tone  due  to 
the  proximity  of  the  stomach  and  colon.  Clinically,  the  splenic 
percussion  area  corresponds  to  an  oblong  patch  of  dulness  lying 
between  the  middle  and  posterior  axillary  lines  and  beneath  the  tenth 
rib,  tenth  interspace,  and  eleventh  rib.  This  superficial  surface  of 
the  spleen,  unlike  the  corresponding  cardiac  and  hepatic  regions, 
affords  dulness  rather  than  true  flatness,  owing  to  its  anatomic 
peculiarities.  In  defining  this  area,  percussion  is  commenced  in  the 
upper  left  axilla  and  carried  downward  along  the  posterior  axillary 
line  until  the  pulmonary  resonance  changes  to  dulness,  at  the  tenth 
rib,  this  point  being  the  clinical  upper  border  of  the  spleen.  Contin- 
uing to  percuss  vertically  downward,  this  dulness  is  replaced  by 
tympany  at  the  lower  margin  of  the  eleventh  rib,  to  which  level  the 
lower  border  reaches.  To  find  the  anterior  border,  percussion  is  car- 
ried along  the  tenth  rib  from  Traube's  area  toward  the  horizontal 
zone  of  dulness  just  delimited,  until  the  note  of  gastric  tympany 
changes  to  dulness,  in  the  midaxillary  line.  The  posterior  border, 
which  cannot  be  mapped  out  successfully,  lies  about  i£  inches 
(3.75  cm.)  to  the  left  of  the  midspinal  line,  the  upper  border  being 
at  the  level  of  the  tenth  thoracic  vertebra  and  the  lower  margin 
lying  next  to  the  left  kidney. 

Aside  from  the  technical  difficulties  inseparable  from  percussion 
of  the  spleen,  the  method  must  needs  be  more  or  less  uncertain 
owing  to  the  many  extrinsic  factors  that  may  decidedly  alter 
the  size  of  the  splenic  area.  The  latter  is  decreased  in  extent  by 
left-sided  emphysema  or  pneumothorax,  as  well  as  by  gaseous 
distention  of  the  stomach  or  colon;  and  it  may  be  increased  in  size 
by  a  long  list  of  extrinsic  causes,  of  which  the  most  important 
are  fluid  or  solid  matter  within  the  stomach  or  within  the  splenic 
flexure  of  the  colon,  consolidation  or  retraction  of  the  base  of  the 
left  lung,  effusion  within  or  great  thickening  of  the  left  pleura,  left- 
sided  intrathoracic  neoplasm,  gastric  cancer,  and  enlargement  of 
the  left  kidney  or  of  the  left  hepatic  lobe. 

In  distinguishing  a  splenic  from  a  renal  tumor,  percussion  deter- 
mines in  the  former  a  lieniform  mass  freely  movable  with  respiration 
and  uniformly  dull  from  well  below  the  left  costal  edge  to  above 
the  upper  limit  of  normal  splenic  dulness  in  the  left  axillary  region; 
in  the  latter  there  is  a  subcostal  reniform  mass  of  limited  motility, 
vertically  traversed  by  a  zone  of  tympany  corresponding  to  the  course 
of  the  colon,  beneath  which  a  tumor  of  the  kidney  is  situated  (Fig. 
223).  A  tumor  of  the  jundus  of  the  stomach,  which  may  be  mis- 
taken for  an  enlarged  spleen,  is  localized  beneath  the  costal  arch  and 


556  PHYSICAL   DIAGNOSIS 

fails  to  show  the  notched  border,  the  sharp  edge,  and  the  distinctive 
contour  of  a  splenic  tumor.  In  enlarged  spleen  versus  tumor  of  the 
lejt  lobe  oj  the  liver,  the  latter  is  suggested  by  finding  a  mass  con- 
tinuous with  hepatic  dulness  to  the  right,  and  one  which  shows  neither 
the  lieniform  shape  nor  the  ready  mobility  (on  bimanual  manipu- 
lation) of  a  splenic  tumor;  moreover,  the  respiratory  displacement 
of  an  hepatic  tumor  is  vertical,  while  that  of  a  splenic  enlargement 
is  diagonal. 


Splenic  tumor.  Renal  tumor. 

Fig.  223. — Percussion  findings  in  splenic  and  in  renal  tumor. 

Auscultation. — A  friction-sound  over  the  splenic  area  may  be 
symptomatic  of  either  perisplenitis  or  pleurisy,  for  the  differentiation 
of  which  other  physical  signs  relating  to  the  spleen  and  pleura  are  to 
be  considered.  In  conditions  of  splenic  enlargement,  especially 
when  associated  with  ptosis  of  the  organ,  there  may  be  a  systolic 
bruit  over  the  spleen,  due  to  torsion  stenosis  of  the  splenic  artery 
(Testi).  Exceptionally,  a  splenic  systolic  murmur  is  also  audible  in 
aortic  regurgitation. 


EXAMINATION   OF   ABDOMEN   AND   ABDOMINAL   VISCERA      557 


EXAMINATION  OF  THE   KIDNEYS 

Clinical  Anatomy. — The  kidneys,  each  of  which  measures 
approximately  4^  inches  (11.25  cm-)  l°ng  by  2\  inches  (6.25  cm.) 
broad,  occupy  the  loin  on  either  side  of  the  spinal  column,  and 
lie  deep  beneath  the  thick  muscles  of  the  lumbar  region  (Fig. 
224).  Topographically,  the  right  kidney  differs  from  the  left  in 
lying  at  a  somewhat  lower  level  and  farther  from  the  spine,  these 
differences  amounting  to  about  \  inch  (1.25  cm.).  Anteriorly 
the  kidneys  lie  beneath  the  costal  borders,  and  extend  vertically  from 


Fig.  224. — Surface  topography  of  the  kidneys. 

the  level  of  the  seventh,  to  somewhat  below  that  of  the  tenth,  cos- 
tal cartilage,  the  inner  border  of  the  right  kidney  being  2  inches 
(5  cm.),  and  that  of  the  left,  i£  inches  (3.75  cm.)  external  to  the 
median  line.  The  infracostal  line  virtually  coincides  with  the  lower 
border  of  the  left  kidney,  but  lies  well  above  this  part  of  the  right 
kidney,  and  the  greater  part  of  both  organs  is  internal  to  Poupart's  ver- 
tical lines.  Posteriorly,  the  kidneys  rest  upon  a  dense  muscular  bed 
composed  of  the  psoas,  quadratus,  transversalis,  and  diaphragm; 
they  extend  vertically  from  the  eleventh  thoracic  to  the  third 


558 


PHYSICAL   DIAGNOSIS 


lumbar  vertebral  spine,  the  lower  borders  being  i$  to  2  inches 
(3.75-5  cm.)  above  the  iliac  crest,  and  the  external  borders  lying 
4  inches  (10  cm.)  from  the  midspinal  line.  The  right  kidney  is  in 
relation  with  the  liver,  the  hepatic  flexure  of  the  colon,  and  the  duod- 
enum, and  the  left  is  adjacent  to  the  fundus  of  the  stomach,  pancreas, 
spleen,  jejunum,  and  splenic  flexure  of  the  descending  colon. 

Inspection. — A  large  renal  tumor  causes  visible  bulging  of  one 
of  the  lateral  regions  of  the  abdomen,  the  deformity  being  especi- 


Calculus. 


Fig.  2240. — Radiograph  of  a  renal  calculus.     (Plate  by  Dr.  W.  F.  Manges.) 

ally  marked  when  the  patient  stands  with  the  body  bent  forward 
so  as  to  relax  the  belly  wall  and  to  favor  descent  of  the  mass. 
A  tumor  first  appearing  in  the  lower  hypochondrium  suggests  primary 
implication  of  the  upper  part  of  the  kidney,  but  a  swelling  first  noticed 
in  the  lumbar  or  iliac  area  points  to  an  initial  invasion  of  the  lower 
renal  surface;  in  either  case  the  enlargement  may  ultimately  become 
enormous  and  distend  any  part,  if  not  the  whole,  of  the  abdomen. 
Save  in  abscess,  which  frequently  causes  a  posterior  swelling  in  the 
loin,  renal  tumors  tend  to  enlarge  anteriorly,  owing  to  the  firm  resist- 


EXAMINATION  OF  ABDOMEN  AND   ABDOMINAL  VISCERA     559 

ance  offered  by  the  muscular  and  osseous  structures  of  the 
back.  Secondary  pressure-changes  associated  with  renal  growths 
include  compression  of  the  right  lung  and  upward  displacement  of 
the  liver  by  right-sided  tumors,  and  the  encroachment  of  left-sided 
neoplasms  upon  the  heart,  the  left  lung,  the  spleen,  and  the  stomach. 

As  factors  of  renal  enlargement  hydronephrosis,  pyonephrosis, 
perinephric  abscess,  and  cystic  degeneration  play  conspicuous,  and 
sarcoma  and  echinococcus  disease  less  prominent,  roles. 

Palpation. — The  patient  may  lie  in  the  dorsal  position  or  stand 
with  the  trunk  inclined  forward,  and  should  breathe  as  deeply  as 
possible,  so  as  to  favor  vertical  displacement  of  the  kidneys  by  the 
action  of  the  diaphragm.  Either  bimanual  palpation,  with  one 
hand  supporting  the  loin  and  the  other  exploring  below  the  costal 
arch,  or  the  method  employed  in  examining  the  spleen  (gripping  the 
flank  with  one  hand)  is  satisfactory  in  palpating  the  kidneys. 

The  renal  reflex  (lumbar  muscle  spasm)  is  a  sign  of  kidney  in- 
flammation, due  to  acute  nephritis,  calculus,  tuberculosis,  and 
similar  processes.  To  elicit  it  the  patient  sits  erect,  with  the  lum- 
bar muscles  relaxed,  and  the  examiner  palpates  the  lumbar  region 
with  a  view  to  determining  increased  muscular  firmness  and  den- 
sity on  the  affected  side  (Pottenger). 

A  normal  kidney  is  sometimes  palpable  in  the  emaciated  subject 
and  in  one  whose  abdominal  parietes  offer  little  or  no  resistance. 
A  renal  tumor  rises  and  falls  with  respiration  to  a  limited  degree ;  it 
is  generally  of  roughly  spherical  shape,  unless  the  growth  happens  to 
enlarge  the  organ  symmetrically,  in  which  event  a  reniform  outline 
may  be  retained;  and  its  consistence  varies  with  the  nature  of  the 
exciting  lesion — it  is  firm  and  resistant  in  sarcoma,  boggy  in  hydro- 
nephrosis and  in  cystic  degeneration,  and  fluctuating  in  abscess  and 
in  hydatid  disease. 

Aside  from  renal  enlargements,  the  condition  of  nephroptosis  is 
the  chief  abnormality  of  the  kidneys  discoverable  by  tactile  sense. 
Nephroptosis,  or  renal  prolapse,  exists  when  the  mobility  of  one  or 
of  both  kidneys  exceeds  the  normal  range,  which  is  approximately 
^  inch  (1.25  cm.).  Although  there  are  precise  technical  differ- 
ences between  a  movable  and  a  floating  kidney  (the  latter  having 
a  mesonephron  and  the  former  none),  the  clinical  criteria  afforded 
by  physical  examination  relate  to  the  range  of  renal  mobility  and 
accessibility.  Thus,  three  clinical  types  of  renal  ptosis  are  recog- 
nized: palpable  kidney,  palpable  but  not  movable  below  the  costal 
margin;  movable  kidney,  whose  entire  anterior  surface  is  easily 
palpable  and  which  can  be  displaced  toward  or  to  the  level  of  the 


560  PHYSICAL   DIAGNOSIS 

navel ;  and  floating  kidney,  which  can  be  readily  pushed  over  to  or 
beyond  the  median  line  and  also  depressed  well  below  the  umbilical 
level.  Prolapse  of  the  kidney,  which  is  more  often  right-  than  left- 
sided,  is  recognized  by  palpating  an  abdominal  reniform  mass  which 
may  be  replaced  to  the  normal  site  of  the  kidney  and  readily  pushed 
from  place  to  place  with  the  hand.  Such  a  tumor  may  or  may  not 
be  larger  than  the  healthy  kidney,  is  usually  sensitive  when  squeezed, 
and  occasionally  shows  the  outline  of  the  hilus  and  perhaps  the  throb 
of  the  renal  artery;  it  is  especially  well  defined  when  the  patient  ceases 
to  breathe  at  the  end  of  a  forced  inspiration,  and  may  tilt  forward 
when  the  subject  takes  the  knee-chest  position  and  drop  backward 
when  dorsal  decubitus  is  assumed.  As  corroborative  signs  of  renal 
displacement  the  so-called  "lumbar  recess"  and  a  tympanitic  percus- 
sion note  over  the  renal  area  in  the  back  are  of  importance. 

An  enlarged  kidney  must  be  distinguished  from  tumors  of  the 
liver  and  of  the  spleen;  a  displaced  kidney,  from  an  enlarged  gall- 
bladder and  from  tumors  of  the  ovary,  the  stomach,  and  the  intestines. 
A  tumor  of  the  liver  lengthens  the  vertical  extent  of  the  hepatic  area, 
tends  to  invade  the  thorax  above  and  to  bulge  it  below,  and  to  pro- 
duce a  subcostal  mass  corresponding  to  the  contour  of  the  liver  and 
moving  freely  with  respiration.  A  tumor  of  the  spleen  is  recognized 
by  its  characteristic  shape,  oblique  position,  free  respiratory  excur- 
sion, uniform  dulness  on  percussion,  and  encroachment  upon  the 
left  thorax  (v.  s.).  A  distended  gall-bladder,  though  to  some 
extent  displaceable,  does  not  remain  so,  but  returns  of  itself  to 
the  edge  of  the  liver  when  the  restraining  pressure  is  removed 
after  it  has  been  pushed  downward;  nor  can  the  gall-bladder  be  pushed 
upward  out  of  reach.  The  respiratory  mobility  of  the  mass  is  con- 
siderable and  its  dulness  is  generally  continuous  with  that  of  the  liver. 
In  the  case  of  an  ovarian  tumor  the  mobility  of  the  mass  is  restricted, 
usually  to  a  level  not  much  higher  than  that  of  the  pelvis;  the  relation 
of  the  tumor  to  the  uterus  can  be  established  by  vaginal  palpation; 
and  its  close  proximity  to  the  anterior  abdominal  wall  can  be  proved 
by  mapping  out  by  percussion  an  area  of  dulness  surrounded  by  a 
zone  of  intestinal  tympany.  Gastric  and  intestinal  tumors  lack  the 
characteristic  mobility  of  a  floating  kidney,  they  do  not  alter  renal 
dulness  in  the  loin,  and  they  can  be  traced  to  their  source  by  inflation 
of  the  stomach  or  of  the  gut,  as  circumstances  indicate. 

Percussion. — In  attempting  percussion  of  the  kidneys  the  diagonal 
decubitus  is  perhaps  the  most  satisfactory  posture  for  the  patient 
to  assume,  in  order  to  relax  the  tense  lumbar  muscles;  but  even  in 
this  position  it  is  impossible  to  reach  the  normal  kidneys  by  percus- 


EXAMINATION  OF  ABDOMEN  AND   ABDOMINAL  VISCERA     561 

sion,  owing  to  their  deep  situation.  The  chief  value  of  percussion 
of  the  kidneys  relaies  to  determining  the  presence  or  absence  of 
colon  tympany  over  a  mass  below  the  left  costal  arch,  which  may 
be  a  tumor  either  of  the  left  kidney  or  of  the  spleen.  (See  Fig.  223.) 
A  kidney  large  enough  to  extend,  or  so  greatly  displaced  as  to  diminish, 
the  renal  area,  can  be  detected  by  palpation.  Posteriorly,  renal  dulness 
is  inseparable  from  that  of  the  overlying  lumbar  muscles,  the  interven- 
ing spinal  column,  and  the  adjacent  spleen  and  liver  (Fig.  225).  A 


_ 

|Eleventh  thoracic 

vertebra 
Twelfth  rib 

Third  lumbar  vertebra 
Descending  colonH  — j'  /  \  -^ ^^•Ascending  colon 

Fig.  225. — The   renal  area  posteriorly,  showing  rectangle  of  percussion  dulness 
between  the  eleventh  thoracic  and  third  lumbar  vertebrae. 

dull  zone,  extending  vertically  from  the  eleventh  thoracic  to  the  third 
lumbar  spine  and  horizontally  for  a  distance  of  about  3  inches 
(7.5  cm.)  on  either  side  of  the  spine,  overlies  the  kidneys,  whose  outer 
and  lower  borders  occasionally  can  be  delimited  from  colon  tympany 
by  percussing  from  the  level  of  the  twelfth  rib  outward  toward  the 
flanks  and  downward  toward  the  iliac  crests.  Dulness  in  the 
scapular  line  below  a  point  i^  inches  (3.75  cm.)  above  the  iliac 
crest  may  mean  an  enlarged  kidney — or  a  colon  packed  with 
feces.  Loss  of  dulness  in  the  renal  area  has  been  found  in  nephrop- 
tosis. 

36 


INDEX 


ABDOMEN,  areas  of,  498 
ascitic,  506 
auscultation  of,  503 
clinical  anatomy,  495 

types,  503 

cutaneous  flexion-folds  of,  497 
dipping  of,  501 
edema  of,  513 

enlarged  and  tortuous  veins  over,  514 
enlargements  of,  509 

above  pubes,  511 

below  left  costal  arch,  511 
right  costal  arch,  510 

from  cancer  of  intestine,  512 
of  peritoneum,  512 

from  distended  bladder,  512 

from  gravid  uterus,  512 

from  leukemic  spleen,  512 

from  ovarian  cyst,  512 

from  tumors,  511 

in  flank,  511 

in  umbilical  region,  511 
enteroptotic,  508 
examination  of,  495 

in  dorsal  position,  500 

in  erect  position,  500 

in  knee-chest  position,  500 

in  lateral  position,  500 

methods,  500 
fat  necrosis  of,  514 
fluctuation  of,  515 
gaseous,  507 
gastroptotic,  508 
inspection  of,  500 
mensuration  of,  502 
movements  of,  512 
muscular  rigidity  of,  515 
obese,  504 
of  pregnancy,  505 
pain  in,  516 
palpation  of,  501 

bimanual,  502 
percussion  of,  502 
puncture  of,  55 
scaphoid,  504 
skin    of,    513.    See.  also    Skin    of 

abdomen. 


Abdomen,  subcutaneous   nodules   of, 

.  5i4 

tissue  of,  513 
tactile  friction  of,  516 
topographic  lines  and  areas,  498 
Abdominal  aorta,  aneurism  of,  493 
diagnosis,  493 
physical  signs,  493 
pulse  in,  493 
clinical  anatomy,  497 
fluid,  examination  of,  58 
friction,  503 
respiration,  93,  95 
thrills,  516 
viscera,  examination  of,  495 

topographic  lines  and  areas,  498 
Abscess,  myocardial,  417 
of  lung,  255 

after  croupous  pneumonia,  203 
clinical  pathology,  255 
diagnosis,  257 
physical  signs,  256 
pericardial,  401 
subphrenic,  294 
Absence  of  septa  between  auricles  and 

ventricles,  474 
Absent  respiration,  158 
Acromion  auscultation,  28 
Actinomycosis,  pulmonary,  264 

physical  signs,  264 
Adenitis,  493 

tracheobronchial,  299 
Adherent  pericardium,  402 
Adhesive  pericarditis,  chronic,  402 
Broadbent's  sign  in,  404 
clinical  pathology,  402 
diagnosis,  405 
Friedreich's  sign  in,  404 
Kussmaul's  sign  in,  404 
physical  signs,  404 
Sander's  sign  in,  404 
pleurisy,  chronic,  283 

clinical  pathology,  283 
diagnosis,  285 
physical  signs,  284 
Adventitious  sounds,  160 
Air-hunger,  Kussmaul's,  102 

563 


564 


INDEX 


Air-passages,    upper,    stenosis   of,   as 

cause  of  dyspnea,  102 
Alar  scapulae,  78 

thorax,  78 

Albinism,  pulmonary,  237 
Alimentary  canal,  test-meals  for  x-ray 

examination  of,  524 
Allorrhythmia,  364 
Allorrhythmic  pulse,  338 
Alternating  pulse,  370 
Alternation  arhythmia,  370 
Amphoric  resonance,  146 

respiration,  154 
Amphoriloquy,  160 
Anacrotism  in  aortic  stenosis,  460 
Anemic  dyspnea,  101 

murmur,  diastolic,  385 
Aneurism,  arteriovenous,  478 
of  abdominal  aorta,  493 
diagnosis,  493 
physical  signs,  493 
pulse  in,  493 
of  aorta,  476 

of  common  carotid  artery,  490 
of  innominate  artery,  490 
of  physical  signs,  489 
of  pulmonary  artery,  490 
of  subclavian  artery,  490 
of  superior  vena  cava,  490 
of  symptoms,  489 
of  thoracic  aorta,  476 
ascending  arch,  480 
buccal  souffle  in,  488 
clinical  pathology,  476 
descending,  480,  481 

arch,  480,  481 
diagnosis,  489 
dissecting,  478 
Drummond's  sign  in,  488 
false,  478 
fusiform,  477 
Glasgow's  sign  in,  488 
Oliver's  sign  in,  486 
physical  signs,  481 
pulse  in,  486 
saccular,  477 
Sansom's  sign  in,  488 
tracheal  elevation  in,  486 

tugging  in,  486 
transverse  arch,  480,  481 
true,  478 
Rasmussen's,  in   chronic   ulcerative 

tuberculosis,  222 
varicose,  479 
Aneurismal  phthisis,  492 

varix,  478 

Angle,  cardiohepatic,  352 
dulness  of,  143 


Angle,  epigastric,  73 
Louis',  71 

pulsations  in,  323 
subcostal,  73 

respiratory  alterations  of,  94 
Angulus  Ludovici,  71 
Anthracosis,  252 

Aorta,  abdominal,  aneurism  of,  493 
diagnosis,  493 
physical  signs,  493 
pulse  in,  493 
clinical  anatomy,  497 
aneurism  of,  476 
ascending,  clinical  anatomy,  311 
dilatation  of,  460 
double,  478 
thoracic,    aneurism    of,    476.     See 

also  A  neurism  of  thoracic  aorta. 
transposition  of,  470 
Aortic  arch,  dynamic  dilatation  of,  451 
area,  356 

incompetence,  relative,  451 
murmurs,  378,  383 
diastolic,  384 
systolic,  384 
regurgitation,  449 
capillary  pulse  in,  453 
clinical  pathology,  449 
Corrigan's  pulse  in,  454 
diagnosis,  457 

difference  in  arm  and  leg  blood- 
pressure  in,  455 
Duroziez's  sign  in,  457 
locomotive  pulse  in,  453 
movable  pulse  in,  453 
Mussel's  sign  in,  452 
physical  signs,  452 
pulse  in,  454 
see-saw  murmur  in,  456 
systolic  blood-pressure  in^  455 
Traube's  sign  in,  457 
venous  pulse  in,  453 
roughening,  384 

sound,  second,  enfeeblement  of,  361 
stenosis,  457 

anacrotism  in,  460 
clinical  pathology,  457 
diagnosis,  461 
physical  signs,  460 
pulse  in,  460 
pulsus  bisferiens  in,  460 

tan  hi*  in,  460 
relative,  460 

valve,  clinical  anatomy,  310 
Apex  pneumonia,  109 
Apex-beat,  317 
absent,  319 
cardiogram  of,  320 


INDEX 


565 


Apex-beat,  character  of,  319 
diastolic  rise  of,  320 
displacement  of,  318 
downward,  318 
left  lateral,  318 
right  lateral,  318 
upward,  318 
downstroke  of,  320 
enfeebled,  319 
exaggeration  of,  319 
upstroke  of,  320 
Apical  systolic  murmur,  378 
Apneumatosis,  248,  249 
Apoplexy  of  lung,  188 

pulmonary,  190 
Appendicitis,    chronic,    Bassler's   sign 

in,  537 

Bastedo's  sign  in,  537 
Appendix,   vermiform,   clinical   anat- 
omy, 533 

Arachnoid  pulse,  344 
Arhythmia,  363 
alternation,  370 
extrasystolic,  364 
fibrillation,  369 
heart-block,  367 
complete,  368 
incomplete,  368 
hemisystolic,  370 
intermittent,  364,  366 
respiratory,  97,  364 
sinus,  364 
youthful  type,  364 

Arm,  upper,  enlargement  of  veins,  105 
Arnold's  phonophore,  26 
Arterial   blood-pressure,   instrumental 

estimation,  31 
murmurs,  392 
diastolic,  393 
systolic,  392 
pulse,  328 
sphygmogram,  40 
tension,  314,  329 
wall,  caliber,  changes  in,  331 

changes  in,  331 
Arteriosclerosis,  331 
Arteriovenous  aneurism,  478 
Artery,    carotid,    common,    aneurism 

of,  490 
epigastric,  deep,   clinical  anatomy, 

497 

iliac,  common,  497 
innominate,  aneurism  of,  490 

clinical  anatomy,  311 
pulmonary,  aneurism  of,  490 

clinical  anatomy,  311 

transposition  of,  475 
subclavian,  aneurism  of,  490 


Arthritis  in  croupous  pneumonia,  203 
Aschner's  oculocardiac  reflex,  337 
Aschoff's  nodules,  419 
Ascitic  abdomen,  506 
Aspiration  pneumonia,  195 
Aspirator,  Potain's,  49 
Asthma,    bronchial,    177.        See   also 
Bronchial  asthma. 

cardiac,  104 

catarrhal,  177 

essential,  177 

grinder's,  252 

idiopathic,  177 

renal,  102 

spasmodic,  177 
Atelectasis,  248 

acquired,  248 

compression,  249 

congenital,  249 

diagnosis,  252 

lobar,  252 

obstruction,  249 

obturation,  183 

physical  signs,  251 
Atelectatic  crepitation,  164 

subcrepitations,  165 
Athlete's  heart,  450 
Atrophic  emphysema  of  lungs,  240,  246 

thorax  of,  80 
Atrophy  of  heart,  475 

progressive  muscular,  thorax  of,  86 

senile,  of  lungs,  246 
Atropin    reaction    in    cardiac    com- 
petency, 333 
Auenbrugger's  sign,.  399 
Auricles  of  heart,  clinical  anatomy,  309 
Auricular  diastole,  314 

extrasystole,  366 

fibrillation,  369 

flutter,  334 

systole,  313 

tachycardia,  334 
Auriculoventricular  bundle  of  His,  313 

extrasystole,  366 

groove,  clinical  anatomy,  310 

node,  313 
Auscultation,  22 

acromion,  28 

immediate,  23,  28 

mediate,  23,  27 

of  abdomen,  503 

of  cardiovascular  system,  355 

of  heart,  355 

of  liver,  549 

of  lungs,  151 
•    of  spleen,  556 

of  stomach,  531 

rod,  1 6 


566 


INDEX 


Auscultation,  stroke,  16 
of  stomach,  531 

technic,  27 

transmanual,  28 

tuning-fork,  28 
Auscultatory  areas,  356 

percussion,  15 
of  stomach,  530 

sphygmomanometry,  33 
Autophonometry,  29 
Axilla,  dulness  in,  143 
Axillary  glands,  enlargement,  113 

line,  anterior,  74 
posterior,  74 

region,  77 
Axis,  celiac,  497 


BAAS'  theory  of  vesicular  breathing, 

i  S3 
Baccelli's  sign,  160 

in  serofibrinous  pleurisy,  275 
Back,  percussion  of,  135 
Band-box   resonance   in   hypertrophic 

emphysema  of  lungs,  244 
Barnard-Hill  sphygmomanometer,  34 
Barrel-chest,  78,  79 
Bassler's  sign,  537 
Bastedo's  sign,  537 
Bathycardia,  317 

Beaded  excrescences  of  valves,  423 
Bell  tympany,  150 
Biermer's  sign,  150 
Biot's  respiration,  99 
Black  phthisis,  252 
Blocked  pleurisy,  5 1 
Blood-pressure,  314 

arm-leg,  in  aortic  regurgitation,  455 

arterial,  instrumental  estimation,  31 

venous,  instrumental  estimation,  36 
Oliver's  method  of  estimating,  36 
Boat-shaped  thorax,  86 
Body,  position  of,  influence  on  cardiac 

physical  signs,  316 
Bookman's  maneuver  in  eliciting  pain 

in  hepatic  area,  542 
Bowies'  stethoscope,  24 
Bradycardia,  336 

Stokes-Adams',  368 
Breast,  chicken-,  82 

funnel-,  83 

keel,  82 

pain  in,  118,  119 

pigeon-,  82 

Breathing,  92.     See  also  Respiration. 
Brenner's  metallic  rub  in  perforation  of 

stomach,  531 
Broadbent's  sign,  324,  404 


Bronchi,  clinical  anatomy,  126 

stenosis  of,  183 
Bronchial  asthma,  177 

clinical  pathology,  177 

Curschmann's  spirals  in,  178 

diagnosis,  179 

Laennec's  perles  in,  178 

physical  signs,  177 
catarrh,  acute,  171 

chronic,  174 
dilatation,  179 
glands,  tuberculosis  of,  299 
riles,  162 
respiration,  153 
Bronchiarctia,  183 
Bronchiectasis,  179 
clinical  pathology,  179 
cylindric,  179 
diagnosis,  182 
fusiform,  179 
globular,  179 
physical  signs,  181 
saccular,  179 
universalis,  179 
Bronchiectatic  cavities,  tympany  in, 

MS 

Bronchiloquy,  160 
Bronchiolectasis,  179 
Bronchitis,  catarrhal,  acute,  171.     See 
also  Catarrhal  bronchitis,  acute. 
chronic,  174.     See  also  Catarrhal 

bronchitis,  chronic. 
fetid,  175 

Dittrich's  plugs  in,  175 
fibrinous,   175.     See  also  Fibrinous 

bronchitis. 
plastic,  175 
putrid, 175 

Bronchocavernous  respiration,  154 
Bronchophony,  159 
Bronchopneumonia,  192 

confluent,  197 

Bronchopneumonic     phthisis,     acute, 
217.     See  also  Phthisis,  acute  bron- 
cho pneumonic. 
Bronchopulmonary   system,   diseases, 

171 

examination,  122 
Bronchorrhea,  175 
Bronchostenosis,  183 
clinical  pathology,  183 
diagnosis,  184 
physical  signs,  184 

Bronchovesicular  respiration,  152,  155 
Brown  induration  of  lungs,  186 
Bruit.     See  also  Murmur. 
buccal,  in  aneurism  of  thoracic  aorta, 
488 


INDEX 


567 


Bruit  d'airain,  150,  292 

de  cuir  neuf,  398 

de  diable,  394 

de  drapeau,  163 

in  fibrinous  bronchitis,  176 

de  galop,  362 

de  moulin,  392 

in  pneumopericardium,  407 

de  pot  fele,  147 

de  rappel.  362 

de  tabourka,  491 

systolic,  over  gall-bladder,  549 
over  spleen,  556 

venous,  over  hepatic  area,  549 

viole,  155 
Bryson's  sign,  96 
Buccal  rales,  162 

souffle    in    aneurism    of    thoracic 

aorta,  488 

Bulging,  unilateral,  of  thorax,  86 
Buth's  method  of  paracentesis  abdomi- 

nis,  58 
Button-hole   mitral   defect   in   mitral 

regurgitation,  440 


CALMETTE'S  ophthalmoreaction,  68 
Cambridge  electrocardiographic  outfit, 

44 

Canter  ryhthm,  362 
Capillary  pulse,  345 

in  aortic  regurgitation,  453 
Caprizant  pulse,  343 
Caput  medusae,  514 
Carcinoma  cells  in  pleural  fluid,  54 

of  lungs,  260 

physical  signs,  262 

of  pleura,  305 

of  stomach,  pain  in,  526 

ac-ray  examination  in,  525 
Cardia,  clinical  anatomy,  519 
Cardiac.     See  Heart. 
Cardiogram,  41 

of  apex-beat,  320 
Cardiography,  37 
Cardiohepatic  angle,  352 

dulness  of,  143 
Cardiopneumatic  rales,  166 
Cardiorespiratory  murmurs,  391 
Cardiovascular    system,    auscultation 

of,  355 

auscultatory  areas  of,  356 
clinical  anatomy,  308 
diseases  of,  396 
examination  of,  308 
inspection  of,  315 
palpation  of,  315 
percussion  of,  350 


Cardiovascular  system,  percussion  of, 

methods  and  technic,  352 
valve  areas  of,  356 
Carditis,  417,  423 
Carnification,  pulmonary,  250 
Carotid    artery,    common,    aneurism 

of,  490 

pulsations,  322 
wave,  42 
Catarrh,  bronchial,  acute,  171 

chronic,  174 
dry,  175 
mucous,  175 
suffocative,  192,  195 
Catarrhal  asthma,  177 
bronchitis,  acute,  171 

clinical  pathology,  171 
diagnosis,  173 
physical  signs,  172 
chronic,  174 

clinical  pathology,  1 74 
diagnosis,  175 
physical  signs,  1 74 
in  croupous  pneumonia,  203 
pneumonia,  192 

clinical  pathology,  192 
diagnosis,  -196 
physical  signs.  195 
Catarrhe  pituiteux,  175 

sec,  175 

Caverniloquy,  160 
Cecum,  clinical  anatomy,  533 
Celiac  axis,  497 
Cells,  cancer,  in  pleural  fluid,  54 

heart  disease,  187 
Cerebrospinal  fluid,  62 

bacteriologic  examination,  63 
chemic  composition,  62 
cytodiagnosis  of,  63 
potassium  content  of,  63 
volume,  62 

Wassermann  reaction  in,  64 
Cervical  glands,  enlargement,  109 
rib,  pressure  of,  on  subclavian  artery, 

492 

veins,  respiratory  turgescence,  129 
Chalicosis,  252 
Chest,  examination  of,  70.     See  also 

Thorax. 

Cheyne-Stokes  respiration,  97 
Chicken-breast,  82 
Chyliform  pleurisy,  269 
Chylopericardium,  406 
Chylothorax,  287 
Cicatrices  fistuleuses  in  fibroid  phthisis, 

235 

of  thorax,  121 
Circulation,  greater,  314 


568 


IXDKX 


Circulation,  lesser,  314 

mechanism  of,  311 

pulmonary,  314 

systemic,  314 
Cirrhosis  of  lung,  213 

after  croupous  pneumonia,  203 
dado's  point,  519 

Clavicles  as  landmarks  of  thorax,  71 
Clavicular  line,  74 
Click,  mucous,  164 
Clubbed  fingers,  121 
Coal-miner's  lung,  252 
Coccygeal  region,  pain  in,  121 
Cog-wheel  respiration,  158 
Collapse,  diastolic,  of  jugular  veins, 

323 

pulmonary,  248 
Collapsing  pulse  in  aortic  regurgitation, 

454 
Colon,  clinical  anatomy,  534 

idiopathic  dilatation,  536         » 

percussion  of,  538 
Coloptosis,  537 
Color  changes  in  skin  of  abdomen, 

5H 
Compensation  of  heart,  430 

ruptured,  431 

Complementary  pleural  sac,  127 
Compression  atelectasis,  249 
Confluent  bronchopneumonia,  197 
Congestion,  pulmonary,  185.    See  also 

Lungs,  congestion  of. 
Contraction,    unilateral,    of    thorax, 

88 

Contusion  pneumonia,  210 
Copenhagen  heart,  438 
Cor  bovinum,  408 

hirsutum,  397 

villosum,  397 
Core  pneumonia,  199 
Corrigan's   button-hole   mitral   defect 
in  mitral  stenosis,  440 

pulse  in  aortic  regurgitation,  454 
Corset-liver,  545 
Costal  arch,  496 

enlargement  of  veins  of,  106 
line  of,  76 
pain  in,  118 

line,  third,  74 
sixth,  76 

respiration,  93,  95 
Cough  phenomenon,  227 

winter,  174 
Courvoisier's  law,  548 
Cracked-pot  resonance,  147 
Crepitant  rales,  163 
Crepitations,  gall-bladder,  549 

subpleural,  168 


Crepitations,  xiphoid,  516 
Crepitus,  162.     See  also  Rdies. 
Cricoclavicular  line,  74 
Crossed  pneumonia,  199 
Croupous  pneumonia,  198 
abscess  of  lung  after,  203 
arthritis  in,  203 
cardiac  sounds  in,  207 
catarrhal  bronchitis  in,  203 
cirrhosis  of  lung  after,  203 
clinical  pathology,  198 
consonating  rales  in,  207 
crepitus  redux  in,  206 
diagnosis,  207 
endocarditis  in,  203 
fibrinous  pleurisy  in,  203 
gangrene  of  lung  after,  203 
myocarditis  in,  203 
pericarditis  in,  203 
phthisis  after,  203 
physical  signs,  204 
pulse  in,  205 
sputum  in,  204 
stage  of  congestion,  200 
of  delayed  resolution,  202 
of  gray  hepatization,  200 
of  purulent  infiltration,  202 
of  red  hepatization,  200 
x-ra.y  examination  in,  205 
Curschmann's    spirals    in    bronchial 

asthma,  178 
Cyanosis,  104 
Cycle,  cardiac,  311 

respiratory,  92 
Crytometry,  30 
Cysts,   echinococcus,   examination  of 

fluid  from,  59 
of  lung,  265 
hydronephrotic,  examination  of  fluid 

from,  59 
of   pancreas,   examination   of   fluid 

from,  59 
ovarian,  examination  of  fluid  from, 

59 
Cytodiagnosis,  50 

of  cerebrospinal  fluid,  63 
of  pleural  fluid,  53 


DEATH-RATTLE,  165 

Decubitus,  influence  of,  on  vocal  frem- 

itus,  132 

Decurtate  pulse,  344 
Degeneration,    myocardial,    granular, 

4i7 
Deglutition  murmur  of  stomach,  531 

pneumonia,  195 
Delirium  cordis,  364 


INDEX 


569 


d'Espine's  sign,  300 
Dextrocardia,  474 
Diabetic  dyspnea,  102 
Diaphragm  phenomenon,  93 
Diaphragmatic  pleurisy,  281 

respiration,  93 
Diastole,  auricular,  314 
prolongation  of,  371 
ventricular,  314 
Diastolic  anemic  murmur,  385 
collapse  of  jugular  veins,  323 
murmurs,  375 
aortic,  384 
arterial,  393 
pulmonic,  388 
rise  of  apex-beat,  320 
Dilatation,  bronchial,  179 
cardiac,  414 
auricular,  417 
clinical  pathology,  414 
diagnosis,  417 
physical  signs,  415 
ventricular,  left,  415 

right,  416 

with  hypertrophy,  414 
with  thinning,  414 
dynamic,  of  aortic  arch,  451 
idiopathic,  of  colon,  536 
of  aorta,  460 
of  lungs,  acute,  247 
Dipping  of  abdomen,  501 
Dissecting  aneurism  of  thoracic  aorta, 

478 
Dittrich's   plugs   in   fetid   bronchitis, 

i7S 
Double  aorta,  478 

murmur,  Duroziez's,  393 

pneumonia,  199 

shock  sound,  Sansom's,  445 
Dropsy  of  lungs,  188 

pericardial,  406 

pleural,  285 
Drummond's    sign    in    aneurism    of 

thoracic  aorta,  488 
Drumstick  fingers,  121 
Dry  catarrh,  175 

rales,  162 

Ductus  arteriosus,  patency  of,  473,  475 
Dudgeon's  sphygmograph,  40 
Dulness,  13,  19 

cardiac,  area  of,  351 
decrease  in,  354 
increase  in,  353 

from   impairment   in   interscapular 
area,  143 

hepatic,  545,  546 

in  axilla,  143 

of  cardiohepatic  angle,  143 


Dulness  of  lung,  141 

apical,  143 

at  base,  143 

paras  ternal,  143 

paravertebral,  143 

sternal,  143 

unilateral,  144 
of    normal    tympany    in    Traube's 

space,  143 
parasternal,  143 
paravertebral,  143 
p'ulmonary,  141.     See  also  Dulness 

of  lung. 
relative,  19 
sternal,  143 
thymus,  492 
vascular,  area  of,  352 
Duodenojejunal  flexure,  clinical  anat- 
omy, 532 

Duodenum,  clinical  anatomy,  532 
Duroziez's  double  murmur,  393 
sign,  394 

in  aortic  regurgitation,  457 
Dyspnea,  100 
anemic,  101 
cardiac,  103 
constant,  100 
diabetic,  102 
expiratory,  100 
functional,  101 
in  fevers,  101 
inspiratory,  100 
mechanical,  102 
mixed,  100 
objective,  100 
obstructive,  102 
paroxysmal,  100 
pulmonary,  103 
stenotic,  102 
subjective,  100 
toxemic,  101 
types,  zoo 
uremic,  101 


ECHINOCOCCTJS  cysts,  examination  of 

fluid  from,  59 
,      of  lung,  265 

Eclat  clangoreaux  diastolique,  398 
Ectasia,  alveolar,  of  lungs,  241 
Ectopia  cordis,  474 
Edema  of  abdomen,  513 
of  lungs,  1 88 

acute  fulminating,  189 

clinical  pathology,  188 

collateral,  189 

congestive,  189 

diagnosis,  190 


570 


INDEX 


Edema  of  lungs,  focal,  189 

Huchard's    paradoxic    percussion 
sound  in,  190 

inflammatory,  189 

physical  signs,  189 

pulse  in,  189 
of  thorax,  106 

general,  109 

local,  1 06 

Effervescence  of  gastric  contents,  531 
Effusion,  pericardial,  serous,  398 
Egophony, 160 
Electrocardiogram,  43 
Electrocardiograph  outfit,  44 
Electrocardiography,  43 
Ellis'    line    in    serofibrinous  pleurisy, 

273 

Embolic  pneumonia,  190 
Embryocardia,  371,  416 
Emphysema,  atrophic,  thorax  of,  80 
compensatory,    hyperresonance    in, 

144 

glass-blowers',  241 
large-lunged,  240,  241 
pulmonary,  240 
acute,  240,  247 
atrophic,  240,  246 
collateral,  246 
compensatory,  240,  246 
complementary,  246 
hypertrophic,  240,  241 

band-box  resonance  in,  244 
clinical  pathology,  241 
diagnosis,  245 
hyperresonance  in,  144 
idiopathic,  240 
interlobular,  248 
interstitial,  240,  248 
intervesicular,  248 
local,  246 
physical  signs,  243 
pseudohypertrophic,  241 
substantive,  241 
true,  241 

vesiculotympany  in,  244 
vicarious,  246 
small-lunged,  240,  246 
Emphysematous  crackling,  163 

thorax,  78 

Empyema  necessitatis,  120,  279 
of  pericardium,  401 
of  thorax,  278 

clinical  pathology,  278 
physical  signs,  280 
pulsating,  279 
Endocardial  murmurs,  372 
Endocarditis,  acute,  421 
diagnosis,  426 


Endocarditis,  acute,  mural,  421 
physical  signs,  425 

chronic,  427 

clinical  pathology,  427 

interstitial,  427 

primary  effects,  430 

secondary  effects,  432 

types  and  relative  incidence,  428 

in  croupous  pneumonia,  203 

malignant,  423 
diagnosis,  426 

ulcerative,  423 

Endotheliocytosis  in  pleural  fluid,  54 
Energy  index,  36 

Enlargement  of  lateral  thoracic  glands, 
114 

of  thymus  gland,  492 
Enteroptosis,  508 
Enteroptotic  abdomen,  508 
Epigastric  angle,  73 

artery,  deep,  clinical  anatomy,  497 

region,  499 
Epigastrium,  enlargement  of,  510 

pain  in,  518 

palpable  thrill  in,  516 

pulsations  in,  324 

Episternal  notch,  pulsations  in,  323 
Erni's  sign,  231 
Erythroblastosis,  fetal,  109 
Essential  asthma,  177 
Ether  pneumonia,  195 
Ewart's  para  vertebral  area,  22 

sign,  399 
Excrescences,  beaded,  of  valves,  423 

verrucose,  of  valves,  423 
Exercise,  effect  of,  on  heart,  355 
Exocardial  murmurs,  389 
Extrasystole,  366 

auricular,  366 

auriculoventricular,  366 

ventricular,  365 
Exudate  in  pleural  fluid,  53 


FACTES,  hepatic,  542 

Falciform  ligament,  539 

Falling-drop  sound,  170 

False  aneurism  of  thoracic  aorta,  478 

Fat  necrosis  of  abdomen,  514 

Fecal  impaction,  537 

Fetal  erythroblastosis,  109 

Fetid  bronchitis,  175 

Dittrich's  plugs  in,  175 
Fetus,  white  pneumonia  of,  238 
Fibrillation  arhythmia,  369 

auricular,  369 

ventricular,  370 
Fibrinous  bronchitis,  175 


INDEX 


571 


Fibrinous  bronchitis,  auscultation  in, 

176 

bruit  de  drapeau  in,  176 
clinical  pathology,  175 
diagnosis,  176 
physical  signs,  176 
pericarditis,  acute,  396 
pleurisy,  283 
acute,  267 

clinical  pathology,  267 
diagnosis,  268 
physical  signs,  267 
in  croupous  pneumonia,  203 
pneumonia,  198 
Fibroid  induration  of  lung,  213 
lung,  213 
phthisis,  234 

cicatrices  fistuleuses  in,  235 
clinical  pathology,  234 
diagnosis,  237 
physical  signs,  235 
pneumonia,  213 

clinical  pathology,  213 
circumscribed,  215 
diagnosis,  216 
diffuse,  213 
physical  signs,  215 
Fibrosis,  myocardial,  417 

of  lung,  237 

Fibrotuberculosis  of  lung,  234 
Finger,  clubbed,  121 
drumstick,  121 
percussion,  13 

Fistula  sound,  pulmonary,  165 
Flack  and  Keith's  node,  313 
Flanks,  clinical  anatomy,  497 
Flat  thorax,  84 
Flatness,  13,  19 

cardiac,  area  of,  350 
hepatic,  547 
pulmonary,  141,  144 
Flexion-folds,  cutaneous,  of  abdomen, 

497 

Flint  murmur,  382 
Floating  kidney,  560 
Fluctuation,  abdominal,  515 

in  diseases  of  pleura  and  lungs,  134 
Fluid  veins,  373 
Fluoroscopy,  65 
Flutter,  auricular,  334 
Foramen  ovale,  patent,  474,  476 
Fossa,  Mohrenheim's,  71 
Fourmentin's  thoracic  index,  70 
Fr6missement  cataire,  327,  443 
Fremitus,  friction,  134,  328 

hydatid,  135,  516 

muscular,  135 

rhonchal,  134 


Fremitus,  succussion,  134 

tussile,  134 

vocal,  131 

decreased,  133 
increased,  133 
Frictio  indux,  276 

redux,  167 
Friction,  abdominal,  503 

fremitus,  134,  328 

intercostal,  168 

pericardial,  328 

peritoneal,  503 
in  peritonitis,  516 

pleural,  166 

pleuropericardial,  168,  328 

shoulder-blade,  168 

shoulder-joint,  168 

tactile,  of  abdomen,  516 

tubercle,  503 

in  tuberculous  peritonitis,  516 
Friction-sounds,  gall-bladder,  549 

perihepatitic,  549 

splenic,  556 

Friedlander  pneumonia,  198 
Friedreich's  sign,  149,  323,  404 
Functional  murmurs,  377 
Funnel-breast,  83 

Funnel-shaped  stenosis,  mitral,  440 
Furrow,  Harrison's,  83 

Sibson's,  73 


GAIRDNER'S  coin-test,  150 
Gall-bladder,  clinical  anatomy,  539 

crepitations,  549 

enlargement  of,  548 

examination  of,  539 

friction-sounds,  549 

inspection  of,  542 

palpation  of,  545 

systob'c  souffle  over,  549 
Gallop  rhythm,  362 
Galloping  consumption,  216 
Gall-stone  crepitus,  503 

x-ray  examination  in,  542 
Galvanometer,  string,  Lewis'  diagram 

of,  45 
Gangrene,  pulmonary,  257 

after  croupous  pneumonia,  203 

circumscribed,  258 

clinical  pathology,  257 

diagnosis,  259 

diffuse,  259 

physical  signs,  259 
Gaseous  abdomen,  507 

pulse,  339 

Gastralgia,  pain  of,  526 
Gastrectasis,  522 


572 


IXDKX 


Gastritis,  pain  of,  526 

Gastrodiaphany,  525 

Gastroptosis,  522 

Gastroptotic  abdomen,  508 

Gerhard t's  sign,  150 

Gibson's  rule  in  pneumonia,  205 

Glands,  lateral,  thoracic,  enlargement 

of,  114 
Glandular  enlargements  about  thorax, 

109 
Glasgow's  sign  in  aneurism  of  thoracic 

aorta,  488 

Glass-blowers'  emphysema,  241 
G16nard's  disease,  508 

method  of  palpating  liver,  544 
Goat-leap  pulse,  343 
Goldscheider's    method    of    threshold 

percussion,  14 

Graham  Steelle  murmur,  473 
Granular  myocardial  degeneration,  417 
Gray  induration  of  lung,  214 
Grinder's  asthma,  252 

rot,  252 
Grocco's  sign,  143 

in  abdominal  cyst,  275 
in  ascites,  275 
in  lumbar  abscess,  275 
in  pregnancy,  275 
in  serofibrinous  pleurisy,  273 
in  subphrenic  abscess,  275 
Groin,  enlarged  glands  in,  514 
Gurgle,  metallic,  3Q2 
Gurgling  in  stomach,  531 

metallic,  in  pneumopericardium,  407 

rales,  165 
Gutta  cadens,  170 

in  pneumothorax,  292 
Gutter-chest,  86 


HAIR  crepitus,  161 
Hairy  heart,  397 
Harrison's  furrow,  83 
Hawksley's  stethoscope,  26 
Heart,  anomalies  of  size,  475 

apex  of,  thrill  at,  327 

area,  displacement  of,  355 

athlete's,  450 

atrophy  of,  475 

auricles  of,  clinical  anatomy,  309 

auscultation  of,  355 

base  of,  309 

pulsations  at  or  near,  323 
thrill  at,  327 

borders,  postural  influences  on,  352 

clinical  anatomy,  310 

compensatory  hypertrophy  of,  430 

Copenhagen,  438 


Heart  cycle,  311 

dilatation  of,  414.     See  also  Dilata- 
tion, cardiac. 
disease,  congenital,  473 
clinical  pathology,  473 
physical  signs,  475 
dulness,  area  of,  351 
decrease  in,  354 
increase  in,  353 
dyspnea,  103 
effect  of  exercise  on,  355 
flatness,  area  of,  350 
hairy,  397 
hypertrophy  of,  407,  475.     See  also 

Hypertrophy,  cardiac. 
in  gastric  cancer,  354 
jinrikisha,  450 

malpositions  of,  congenital,  474 
movements,  312 
orifices  of,  310 

ruptured  compensation  of,  431 
valves  of,  310 
Heart-beat,  311 

myogenic  theory,  312 
neurogenic,  312 
Heart-block,  368 
arhythmia,  367 
Heart-disease  cells,  187 
Heart-sounds,  356 
adventitious,  372 
first,  357 

at  apex,  accentuation  of,  359 

enfeeblement  of,  360 
reduplication  of,  362 
in  croupous  pneumonia,  207 
intensity  of,  changes  in,  358 
psychic,  378 

quality  of,  changes  in,  359 
reduplication  of,  362 
second, 358 
at  base,  accentuation  of,  360 

enfeeblement  of,  361 
reduplication  of,  363 
third,  357 

Hemisystolic  arhythmia,  370 
Hemopericardium,  406 
Hemopneumopericardium,  406 
Hemopneumothorax,  287 
Hemorrhage,  concealed,  of  phthisis,  222 
pericardial,  406 
pleural,  286 

Hemorrhagic  infarction  of  lungs,  too 
clinical  pathology,  190 
diagnosis,  192 
physical  signs,  192 
pleurisy,  269 
Hemothorax,  286 
Hen-cluck  stertor,  99 


INDEX 


573 


Hepatic  facies,  542 

flexure,  clinical  anatomy,  534 
Hepatization,  white,  of  lung,  237 
Hepatoptosis,  548 
Herrick's  method  of  paracentesis  in 

diagnosis  of  pneumoperitoneum,  56 
Hill-Barnard  sphygmomanometer,  34 
Hippocratic  succussion  sound,  170 
His's  bundle,  313 
Hoover's   method   of   inspection   and 

palpation  of  subcostal  angle,  94 
Hour-glass  stomach,  523 
Huchard's  paradoxic  percussion  sound, 

190 

Humming-top  murmur,  394 
Hydatid  fremitus,  135 

resonance,  19 

thrill,  516 
Hydronephrotic  cysts,  examination  of 

fluid  from,  59 
Hydropericardium,  406 
Hydropneumopericardium,  406 
Hydropneumothorax,  287 
Hydrops  adiposus,  269 

chylosus,  269,  287 

ex  vacuo,  286 
Hydrothorax,  285 
Hyperemia  of  lungs,  185 
Hyperresonance  in  compensatory  em- 
physema, 144 

in  hypertrophic  emphysema,  144 

pulmonary,  144 

pulmonary   relaxation   as    cause, 

MS 
Hyperresonant  percussion-sounds,  13, 

19 

Hypertension,  36 
Hypertrophy,  cardiac,  407,  475 

auricular,  411 

circumscribed,  408 

clinical  pathology,  407 

compensatory,  430 

concentric,  408 

diagnosis,  412 

eccentric,  408 

general,  408,  410 

partial,  408 

physical  signs,  411 

primary  congenital,  410 

simple,  408 

ventricular,  left,  410 

right,  410 
ox-heart,  408 
Hypochondriac  region,  77 

pain  in,  519 
Hypochondrium,  left,  pain  in,  117 

right,  pain  in,  117 
Hypogastric  region,  499 


Hypogastric  region,  pain  in,  518 
Hypotension,  36 


ILEOCECAL  valve,  clinical  anatomy,  533 
Ileolumbar  region,  pain  in,  519 
Ileum,  clinical  anatomy,  532 
Iliac  arteries,  common,  497 

region,  499 

spines,  anterior  superior,  496 
Illness,  serum,  52 
Incisura  angularis  of  stomach,  clinical 

anatomy,  521 
Index,  energy,  36 

thoracic,  Fourmen tin's,  70 
Infarction,  hemorrhagic,  of  lungs,  190. 

See  also  Hemorrhagic  infarction  oj 

lungs. 

Infiltration,  serous,  of  lung,  188 
Inflated  thorax,  78 
Infra-axillary  region,  77 
Infraclavicular  region,  77 
Infracostal  line,  76,  498 
Inframammary  region,  77 
Infrascapular  line,  77 

region,  77 

Inguinal  region,  499 
Innominate  artery,  aneurism  of,  490 
clinical  anatomy,  311 

veins,  clinical  anatomy,  311 
Inoscopy  of  pleural  fluid,  54 
Inspection,  12 

of  abdomen,  500 

of  cardiovascular  system,  315 

of  gall-bladder,  542 

of  intestines,  534 

of  kidneys,  558 

of  liver,  542 

of  lungs,  1 28 

of  spleen,  551 

of  stomach,  521 
Instrumental  percussion,  13 
Intensity  of  sound,  18 
Intercostal    spaces    as    landmarks   of 

thorax,  72 
pulsations  in,  323 
thrill  at,  327 

Interscapular    area,    impairment    in, 
dulness  from,  143 

region,  77 

Interspinal  line,  498 
Interstitial  pneumonia,  chronic,  213 

See  also  Fibroid  pneumonia. 
Interventricular  groove,  clinical  anat- 
omy, 310 

septum,  defects  of,  473,  475 
Intestinal  obstruction,  535 

sounds,  503 


574 


INDKX 


Intestines,  clinical  anatomy,  532 
examination  of,  532 
inspection  of,  534 
large,  clinical  anatomy,  533 

x-ray  examination  of,  534 
malignant  disease,  538 
palpation  of,  534 
percussion  of,  538 
peristalsis  of,  512 
small,  clinical  anatomy,  532 

percussion  of,  538 

ptosis  of,  537 


JAQUET'S  sphygmocardiograph,  38 

Jejunum,  clinical  anatomy,  532 

Jinrikisha  heart,  450 

Joint,  xiphisternal,  71 

Jug  sound,  147 

Jugular  veins,  diastolic  collapse,  323 

engorgement,  326 

pulsations,  322 

Jiirgensen's    sign    in    acute    broncho- 
pneumonic  phthisis,  219 


KAOLINOSIS,  253 

Katzenschiirren,  327 

Keel  breast,  82 

Keith  and  Flack's  node,  313 

Kent's  node,  313 

Kidneys,  clinical  anatomy,  557 

enlarged,  560 

examination  of,  557 

floating,  560 

inspection  of,  558 

movable,  559 

palpable,  559 

palpation  of,  559 

percussion  of,  560 

puncture  of,  64 
Knife-grinder's  phthisis,  252 
Koch's  tuberculin  test,  67 
Koranyi's  method  of  percussion,  17 

spinal  zones,  21 
Kussmaul's  air-hunger,  102 

sign,  326,  404 
Kyphosis,  82 


LAENNEC'S  catarrhe  pituiteux,  175 
sec,  175 

perles  in  bronchial  asthma,  178 

theory  of  vesicular  breathing,  153 
Laryngeal  crepitus  in  phthisis,  233 

paralysis  in  mitral  stenosis,  442 

rales,  162 
Larynx,  displacement  of,  129 


Law,  Courvoisier's,  548 
Leaden  overcast,  316 
Leopard's  growl,  100 
Lewis'   diagram    of    string    galvano- 
meter, 45 
Lian's  point,  56 
Ligament,  falciform,  539 
Ligaments,  Poupart's,  496 
Ligne  blanche  abdominale,  514 
Line,  axillary,  anterior,  74 
posterior,  74 

clavicular,  74 

costal,  third,  74 
sixth,  76 

cricoclavicular,  74 

Ellis',  in  seronbrinous  pleurisy,  273 

infracostal,  76,  498 

infrascapular,  77 

interspinal,  498 

mammillary,  74 

midaxillary,  74 

midclavicular,  74 

midsternal,  74 

of  costal  arch,  76 

of  transmission  of  murmurs,  375 

of  twelfth  thoracic  vertebra,  77 

parasternal,  74 

Poupart's,  498 

scapular,  74 
spinal,  77 

sternal,  74 
Linea  alba,  497 

albicantes,  514 

gravidarum,  514 

nigra,  497 
Linese  semilunares,  497 

transversae,  497 
Lithosis,  252 
Litten's  sign,  93 
Liver,  areas  of  dulness  and  flatness,  545 

auscultation  of,  549 

clinical  anatomy,  539 

consistence  of,  544 

contour  of,  544 

corset-,  545 

decrease  in  size  of,  547 

descent  of,  543 

displacement  of,  548 

enlargement  of,  543,  547 

examination  of,  539 

inspection  of,  542 

pain  in  region  of,  542 

palpation  of,  Gl£nard's  method,  544 

percussion  of,  545 

prolapse  of,  548 

pulsations  of,  324,  542 

puncture  of,  64 

surface  topography,  540 


INDEX 


575 


Liver,  tenderness  in  region  of,  542 
venous  bruit  over,  549 

murmur  over,  549 
Lobar  atelectasis,  252 

pneumonia,  198 
Lobular  pneumonia,  192 
Locomotive  pulse  in  aortic  regurgita- 

tion,  453 
Loin,  clinical  anatomy,  497 

pain  in,  519 

Lombardi's  sign  of  apical  phthisis,  226 
Lordosis,  82 
Lorenz's    sign    in    chronic    ulcerative 

phthisis,  224 
Louis'  angle,  71 

pulsations  in,  323 
Lumbar  muscle  spasm,  559 
puncture,  60 
region,  499 

pain  in,  120 
Lungs,    abscess    of,     255.     See    also 

Abscess  of  lung. 
actinomycosis  of,  264 
physical  signs,  264 
albinism  of,  237 
alveolar  ectasia,  241 
anterior  borders,  123,  124 
apices  of,  1 23 
pain  at,  117 
percussion  of,  136 
apoplexy  of,  188,  190 
atrophy  of,  senile,  246 
auscultation  of,  151 
borders  of,  changes  in  mobility  and 

position,  139 
normal  limits,  139 
upper,  139 

brown  induration,  186 
carcinoma  of,  260 

physical  signs,  262 
carnification  of,  250 
catarrhal  pneumonia,  192 
cavities  of,  tympany  in,  145 
circulation  of,  314 
cirrhosis  of,  213 

after  croupous  pneumonia,  203 
clinical  anatomy,  122 
coal-miner's,  252 
collapse  of,  248 
congestion  of,  185 
acute,  185,  187 
chronic,  186,  187 
clinical  pathology,  185 
collateral,  186 
diagnosis,  188 
hypostatic,  186,  188 
mechanical,  186 
passive,  186 


Lungs,  congestion  of,  physical  signs, 

187 

costal  surfaces,  122 
croupous  pneumonia,  198 
dilatation  of,  acute,  247 
dropsy  of,  188 
dulness  of,   141.     See  also  Dulness 

of  lung. 

dyspnea  of,  103 
echinococcus  cyst,  265 
edema    of,    188.     See    also    Edema 

of  lungs. 
emphysema    of,     240.        See    also 

Emphysema,  pulmonary. 
fever,  198 
fibroid,  213 

induration,  213 
fibrosis,  of  237 
fissures  of,  125 
fistula  sound,  165 
flatness  of,  141 
gangrene  of ,  257.     See  also  Gangrene, 

pulmonary. 
gray  induration,  214 
hemorrhagic  infarction,  190.       See 

also    Hemorrhagic    infarction    of 

lungs. 

hilus  of,  1 23 
hyperemia  of,  185 
inspection  of,  1 28 
lobes  of,  125 

limits,  126 
lower  borders,  1 24 
mediastinal  surfaces,  122 
mobility  of,  gaging,  by  pulmonary 

borders,  139 
palpation  of,  130 
percussion  of,  135 

comparative,  136 
potter's,  253 
puncture  of,  64 
reflex,  151 
root  of,  123 
sarcoma  of.  263 
sclerosis  of,  213 
senile  atrophy,  246 
serous  infiltration,  188 
syphilis  of,  237.     See  also  Syphilis, 

pulmonary. 

tuberculofibrosis  of,  234 
tumors  of,  260 
tympany  of,  144 
white  hepatization,  237 
Lymphadenitis,  mediastinal,  298 

physical  signs,  299 

Smith's  murmur  in,  300 

suppurative,  299 
Lymphocytosis  in  pleural  fluid,  53 


576 


INDEX 


MALIGNANT  endocarditis,  423 

diagnosis,  426 
Mammary  region,  77 
veins,  enlarged,  105 
Mammillary  line,  74 
McBurney's  point,  519 
Mediastinal  lymphadenitis,  298 
physical  signs,  299 
Smith's  murmur  in,  300 
suppurative,  299 
pleurisy,  283 
Mediastinitis,  296 
acute,  296 
chronic,  296 
suppurative,  297 
Mediastinopericarditis,  402 

indurative,  296 
Mediastinum,  anterior,  128 
clinical  anatomy,  127 
diseases  of,  171 
middle,  128 
posterior,  128 
superior,  128 
tumors  of,  300.     See  also  Tumors 

of  mediastinum. 
Meningeal  respiration,  99 
Mensuration  of  abdomen,  502 

of  thorax,  29 
Mesocardia,  474 
Metallic  gurgle,  392 

in  pneumopericardium,  407 
tinkling,  170 

Micrococcus  Pasteuri,  198 
Midaxillary  line,  74 
Midclavicular  line,  74 
Midspinal  line,  74 
Midsternal  line,  74 

Milk-spots  .  in    serofibrinous    pericar- 
ditis, 398 

Mirror-image  of  precordial  region,  318 
Mitral  area,  356 
murmurs,  381 
presystolic,  382 
systolic,  383 
regurgitation,  434 
clinical  pathology,  434 
diagnosis,  438 
muscular  type,  435 
organic  type,  434 
physical  signs,  436 
pulmonary  pulse  in,  437 
radial  pulse  in,  437 
stenosis,  439 

clinical  pathology,  439 
Corrigan's  button-hole  mitral  de- 
fect in,  440 
diagnosis,  448 
first  stage  of,  444 


Mitral  stenosis,  fremissement  cataire 

in,  443 

funnel-shaped,  440 

physical  signs,  443 

pulse  in,  444 

recurrent  laryngeal   nerve  paral- 
ysis in,  442 

relative,  441 

Samson's    double    shock    sound 

in,  445 

second  stage  of,  446 
soft-valve,  441 
third  stage  of,  447 
valve,  clinical  anatomy,  310 
Mohrenheim's  fossa,  71 
Moist  rales,  163 
Money-chink  resonance,  147 
Moro's  reaction,  69 
Morris'  point,  pain  at,  518 
Mortification,  pulmonary,  257 
Mouneret's  pulse,  339 
Mountain  sickness,  101 
Mouse-tail  pulse,  344 
Movable  kidney,  559 

pulse  in  aortic  regurgitation,  453 
Mucous  catarrh,  175 
click,  164 
rales,  165 

Multiple  murmurs,  388 
Munro's  point,  56 
Murmurs.     See  also  Bruit. 
analysis  of,  380 
anemic,  385 

diastohc,  385 
aortic,  378,  383 
diastolic,  384 
systolic,  384 
arterial,  392 
diastolic,  393 
systolic,  392 
cardiorespiratory,  391 
clinical  attributes,  374 
deglutition,  of  stomach,  531 
diastolic,  375 
Duroziez's,  393 
endocardial,  372 
exocardial,  389 
Flint,  382 
functional,  377 
Graham  Steelle,  473 
humming-top,  394 
intensity  and  quality,  375 
line  of  transmission,  375 
mid-diastolic,  375 
mitral,  381 

presystolic,  382 
systolic,  383 
multiple,  388 


INDEX 


577 


Murmurs    of   high    pressure   in   pul- 
monary artery,  473 
organic,  372 
pericardia!,  389 

intensity  and  quality,  390 

rhythm  of,  390 
pericarditic,  presystolic,  383 
point  of  maximum  intensity,  375 
post-systolic,  375 
protodiastolic,  375 
psychic  heart,  378 
pulmonic,  diastolic,  388 

systolic,  387 
rhythm  of,  374 
Rogers',  475 
safety-valve,  378 

see-saw,  in  aortic  regurgitation,  456 
Smith's,  in  mediastinal  lymphaden- 
itis, 300 
systolic,  374 

apical,  378 

pulmonic,  378 

tricuspid,  378 
transmission  of,  375 
tricuspid,  385 

presystolic,  385 

systolic,  385 
vascular,  392 
venous,  394 

over  hepatic  area,  549 
Muscle  sounds,  161 

spasm,  lumbar,  559 
Muscular  atrophy,  progressive,  thorax 

of,  86 

fremitus,  135 
rigidity  of  abdomen,  515 
Musset's  sign  in  aortic  regurgitation, 

452 

Mute  pneumothorax,  293 
Mj'ocardial  abscess,  417 
degeneration,  granular,  417 
fibrosis,  417 
Myocarditis,  417 
acute,  417 

interstitial,  418 

parenchymatous,  417 

suppurative,  418 
chronic,  418 
clinical  pathology,  417 
diagnosis,  420 

in  croupous  pneumonia,  203 
physical  signs,  420 
Myoidema  in  phthisis,  231 


NAtTNYN's  sign,  518 
Navel,  497 

condition  of,  514 

37 


Neck,  pulsations  in,  322 

venous  suffusion,  129 
Necropneumonia,  257 
Necrosis,  fat,  of  abdomen,  514 
Nephroptosis,  559 
Neuroses,    functional,    as    cause    of 

functional  dyspnea,  101 
Nicholson's  sphygmomanometer,  31 
Nipple  as  landmark  of  thorax,  73 
Nodal  rhythm,  366,  369 
Node,  auriculoventricular,  313 

Keith  and  Flack's,  313 

Kent's,  313 

sino-auricular,  313 

Tawara's  313 
Nodules,  Aschoff's,  419 

subcutaneous,  of  abdomen,  514 
Noise,  water- whistle,  165 
in  pneumothorax,  292 


OBESE  abdomen,  504 
Obturation  atelectasis,  183 
Occipital  glands,  enlargement,  no 
Oculocardiac  reflex,  337 
Oligopnea,  97 

Oliver's  method  of  estimating  venous 
pressure,  36 

sign,  328 

Ophthalmoreaction,  Calmette's,  68 
Organ-pipe  arrangement  of  intestinal 

loops,  536 

Organic  murmurs,  372 
Orthopnea,  100 
Osteal  resonance,  19 
Ovarian  cysts,    examination    of    fluid 

from,  59 
Ox-heart  hypertrophy,  408 


PAIN  at  apex  of  lung,  117 
at  Morris'  point,  518 
at  Robson's  point,  518 
gastric,  526 
in  abdomen,  516 
in  breast,  117 
in  cancer  of  stomach,  526 
in  coccygeal  region,  121 
in  costal  arch,  118 
in  epigastrium.  518 
in  hepatic  region,  542 
in  hypochondriac  regions,  519 
in  hypogastric  region,  518 
in  ileolumbar  region,  519 
in  lateral  wall  of  thorax,  119 
in  left  hypochondrium,  117 

shoulder,  117 
in  loins,  519 


INDEX 


Pain  in  lumbar  region,  1 20 

in  posterior  wall  of  thorax,  119 

in  precordia,  117 

in  right  hypochondrium,  117 
shoulder,  117 

in  sacral  region,  220 

in  sacrum,  519 

in  splenic  region,  553 

in  thorax,  117 

in  tumors  of  stomach,  526 

in  umbilical  region,  518 

of  gastralgia,  526 

of  gastric  ulcer,  526 

of  gastritis,  526 

sternal,  117 
Palpable  kidney,  559 
Palpation,  n 

of  abdomen,  501 

of  cardiovascular  system,  315 

of  gall-bladder,  545 

of  intestines,  534 

of  kidneys,  559 

of  liver,  Glenard's  method,  544 

of  lungs,  130 

of  spleen,  551 

of  stomach,  525 
Palpatory  percussion,  15 
Pancarditis,  423 
Pancreas,  clinical  anatomy,  549 

cysts  of,  examination  of  fluid  from, 

,.59. 
physical  examination,  549 

Parabronchial     consolidations,     tym- 

pany  from,  146 
Paracentesis,  47 

abdominis,  55 

Buth's  method,  58 
diagnostic,  55 
therapeutic,  56 

Herrick's  method  of,  in  diagnosis  of 
pneumoperitoneum,  56 

lumbar,  60 

of  kidney,  64 

of  liver,  64 

of  lung,  64 

of  pericardial  sac,  54 

of  pleural  cavity,  50 

of  spleen,  64 

technic,  47 

visceral,  64 
Paralytic  thorax,  78 
Parasternal  dulness,  143 

line,  74 

Paravertebral  dulness,  143 
Parietal  pleura,  126 
Parotid  gland,  enlargement,  113 
Paroxysmal  dyspnea,  100 

tachycardia,  336 


Patency  of  ductus  arteriosus,  473,  475 
Patent  foramen  ovale,  474,  476 
Pectoriloquy,  159 

whispering,  159 
Pectus  carinatum,  82 

excavatum,  83 
Pendulum  rhythm,  371 
Percussion,  12 

auscultatory,  15 
of  stomach,  530 

finger,  13 

immediate,  13,  14 

in  intestinal  obstruction,  539 

instrumental,  13 

Koranyi's  method,  17 

mediate,  13 

of  abdomen,  502 

of  anterior  chest-wall,  135 

of  apices  of  lungs,  136 

of  back,  135 

of  cardiovascular  system,  350 
methods  and  technic,  352 

of  colon,  538 

of  intestines,  538 

of  kidneys,  560 

of  lateral  regions  of  thorax,  136 

of  liver,  545 

of  lungs,  135 

comparative,  136 

of  small  intestine,  538 

of  spleen,  554 

of  stomach,  529 

palpatory,  15 

respiratory,  136 

sense  of  resistance,  17,  1 8 

spinal,  20 

technic,  13 

threshold,  Goldscheider's  method,  14 

zones,  spinal,  21 
Percussion-sound,  attributes,  17 

duration,  18 

Huchard's,  190 

hyperresonant,  13,  19 

intensity,  18 

pitch,  17 

quality,  17 

resonant,  13,  1 8 

special  tonal  changes  of,  147 

tonal  properties,  18 

tympanic,  13,  19 
Perez's  sign,  168 
Perforation  of  stomach,  metallic  rub  in, 

Peribronchial  pneumonia,  192 
Pericardial  abscess,  401 

dropsy,  406 

effusion,  serous,  398 

fluid,  examination,  55 


INDEX 


579 


Pericardial  friction,  328,  389 
intensity  and  quality,  390 
rhythm  of,  390 
hemorrhage,  406 
sac,  puncture  of,  54 
succussion  sounds,  392 
Pericardicentesis,  54 
Pericarditic  presystolic  rumble,  383 

pseudocirrhosis,  297 
Pericarditis,  396 

adhesive,    chronic,    402.     See    also 

Adhesive  pericarditis,  chronic. 
external,  297 
fibrinous,  acute,  396 

clinical  pathology,  396 
diagnosis,  398 
physical  signs,  397 
in  croupous  pneumonia,  203 
internal,  297 
plastic,  acute,  396 
purulent,  401 

clinical  pathology,  401 
physical  signs,  402 
serofibrinous,  398 

Auenbrugger's  sign  in,  399 
clinical  pathology,  398 
diagnosis,  401 
Ewart's  sign  in,  399 
milk-spots  in,  398 
physical  signs,  399 
Rotch's  sign  in,  400 
Pericardium,  adherent,  402 

empyema  of,  401 
Pericolitis  sinistra,  537 
Perihepatitic  friction-sound,  549 
Peristalsis  of  stomach  and  intestine, 

512 

Peristaltic  unrest,  513 
Peritoneal  friction,  503 
in  peritonitis,  516 
Phonometry,  28 
Phthisical  thorax,  78 
Phthisis,  acute  bronchopneumonic,  217 
Jiirgensen's  sign  in,  219 
physical  signs,  218 
pneumonic,  216 

clinical  pathology,  216 
diagnosis,  219 
physical  signs,  218 
after  croupous  pneumonia,  203 
aneurismal,  492 
apical,  Lombardi's  sign,  226 
black,  252 
chronic  ulcerative,  220 

chloasma  phthisicorum  in,  226 
clinical  pathology,  220 
concealed  hemorrhage  of,  222 
diagnosis  233 


Phthisis,  chronic  ulcerative,  laryngeal 

crepitus  in,  233 
Lorenz's  sign  in,  224 
myoidema  in,  231 
periods  of,  224 
physical  signs,  224 
Rothschild's  sign  in,  224 
signe  du  tapotage  in,  231 
striae  vasculares  in,  226 
valvular  heart  disease  in,  222 
Williams'  sign  in,  227 
fibroid,     234.      See    also    Fibroid 

phthisis. 
florida,  216 
galloping,  216 
knife-grinder's,  252 
Sabourin's  sign,  226 
slow,  220 
stone-cutter's,  252 
Physical  diagnosis,  methods  and  tech- 

nic,  ii 

Physiologic  venous  pulse,  42 
Pick's  disease,  297 
Pigeon-breast,  82 
Pirquet's  tuberculin  test,  67 
Pistol  pulse  in  aortic  regurgitation,  454 
Pitch  of  sound,  1 7 
Pitres'  signe  du  sou,  151 
Plastic  bronchitis,  175 
pericarditis,  acute,  396 
pleurisy,  267 

chronic,  283 

Pleura,  carcinoma  of,  295 
clinical  anatomy,  126 
parietal,  126 
sarcoma  of,  296 
tumors  of,  295 
visceral,  127 

Pleural  cavity,  puncture,  50 
dropsy,  285 

fluid,  cancer  cells  in,  54 
cytodiagnosis,  53 
endotheliocytosis  in,  54 
examination,  53 
exudate  in,  53 
inoscopy  of,  54 
lymphocytosis  in,  53 
polynucleosis  in,  54 
transudate  in,  53 
friction,  1 66 
hemorrhage,  286 
space,  complementary,  127 
Pleur6sie  bloqude,  51 
Pleurisy,  266 
acute  dry,  267 
adhesive,  chronic,   283.       See  also 

Adhesive  plettrisy,  chronic. 
blocked,  51 


INDEX 


Pleurisy,  chyliform,  269 

circumscribed,  281 

diaphragmatic,  281 

encapsulated,  282 

encysted,  282 

fibrinous,  283 
acute,  267.      See  also  Fibrinous 

pleurisy,  acute. 
in  croupous  pneumonia,  203 

hemorrhagic,  269 

interlobar,  282 

mediastinal,  283 

plastic,  267 
chronic,  283 

pulsating,  279 

purulent,  278.    See  also  Empyema. 

serofibrinous,  268.      See  also  Sero- 
fibrinous  pleurisy. 

with  effusion,  268 
Pleuritis,  266 

sicca,  267 
Pleurocentesis,  50 
Pleuropericardial  friction,  168,  328 
Pleuropneumonia,  203 
Pneumochysis,  188 
Pneumonia,  apex,  199 

aspiration,  195 

catarrhal,  192.      See  also  Calarrhal 
pneumonia. 

central,  199 

contusion,  210 

core,  199 

crossed,  199 

croupous,  198.      See  also  Croupous 
pneumonia. 

deglutition,  195 

disseminated,  192 

double,  199 

embolic,  190 

errans,  199 

ether,  195 

fibrinous,  198 

fibroid,  213.      See  also  Fibroid  pneu- 
monia. 

Friedlander,  198 

Gibson's  rule  in,  205 

hypostatic,  187 

interstitial,  chronic,  213.    See  also 
Fibroid  pneumonia. 

lobar,  198 

lobular,  192 

massive,  199 

migrans,  199 

peribronchial,  192 

purulent,  255 

stripe,  199 

superficial,  199 

syphilitic,  237 


Pneumonia,  toxic,  208 

traumatic,  210 

typhoid,  208 

wandering, 199 

white,  237 

of  fetus,  238 
Pneumonic  phthisis,  acute.    See  also 

Phthisis,  acute  pneumonic. 
Pneumonitis,  198 
Pneumonoconiosis,  252 

clinical  pathology,  252 

diagnosis,  255 

physical  signs,  255 
Pneumopericardium,  406 

bruit  de  moultn  in,  407 

metallic  gurgling  in,  407 

physical  signs,  407 
Pneumoperitoneum,  508 

diagnosis  of,   Herrick's   method   of 

paracentesis  in,  56 
Pneumorrhagia,  190 
Pneumothorax,  287 

artificial,  52 

bilateral,  289 

bruit  d'airain  in,  292 

circumscribed  or  limited,  289 

clinical  pathology,  287 

closed,  289 

diagnosis,  292 

general  or  complete,  289 

gutta  cadens  in,  292 

mute,  293 

open,  289 

physical  signs,  290 

succussio  Hippocratis  in,  292 

tympany  in,  146 

valvular,  289 

ventilated,  289 

water- whistle  noise  in,  292 
Pneumotyphus,  208 
Point,  Clado's,  519 

Lian's,  56 

McBurney's,  519 

Morris',  518 

Munro's,  56 

Robson's,  518 

spleen,  553 

Voillemier's,  519 
Polynucleosis  in  pleural  fluid,  54 
Polypnea,  97 

Polypous  lesions  of  valves,  423 
Posture,  influence,  on  cardiac  signs,  316 
on  percussion  sound,  139 
on  pre'cordial  borders,  352 
on  vocal  fremitus,  132 
Potain's  aspirator,  49 
Potassium    content    of    cerebrospinal 

fluid,  63 


INDEX 


Potter's  lung,  253 
Poupart's  ligaments,  496 

lines,  498 
Precordia,  bulging  of,  316 

clinical  anatomy,  309 

flattening  or  depression  of,  317 

pain  in,  117 
Precordial  area,  pulsations  in,  323 

contour,  316 

Pregnancy,  abdomen  of,  505 
Progressive  muscular  atrophy,  thorax 

of,  86 

Prolapse  of  liver,  548 
Pseudocirrhosis,  pericarditic,  297 
Pseudolipoma,  Verneuil's,  90 
Psychic  heart  murmur,  378 
Pterygoid  thorax,  78 
Ptosis  of  small  intestine,  537 
Pubic  region,  499 

spines,  496 

symphysis,  496 
Puff,  veiled,  Laennec's,  155 
Pulmonary  artery,  aneurism  of,  490 
clinical  anatomy,  311 
transposition  of,  475 

edema,  188 

pulse  in  mitral  regurgitation,  437 

regurgitation,  471.      See  also  Regur- 
gitation, pulmonary. 

resonance,  137.      See  also  Resonance, 
pulmonary. 

splenization,  187 

stenosis,   467.       See  also  Stenosis, 
pulmonary. 

tympanites,  145 
Pulmonic  area,  356 

murmurs,  diastolic,  388 
systolic,  378,  387 

sound,  second,  accentuation  of,  361 
weakening  of,  362 

valve,  clinical  anatomy,  310 
Pulsating  empyema,  279 

pleurisy,  279 
Pulsations,  abnormal  areas  of,  321 

at  Louis'  angle,  323 

at  or  near  base  of  heart,  323 

carotid,  322 

circumscribed  areas  of,  in  diseases 
of  lungs  and  pleura,  1 29 

in  epigastrium,  324 
postsystolic,  324 
systolic,  324 

in  episternal  notch,  323 

in  intercostal  spaces,  323 

in  neck,  322 

in  precordial  area,  323 

of  jugular  veins,  322 

of  liver,  324,  542 


Pulsations  of  spleen,  553 
Pulse,  allorrhythmic,  338 
alternating,  338,  370 
arachnoid,  344 
arterial,  328 
asymmetry,  of  345 
capillary,  345,  453 
caprizant,  343 
collapsing,  454 
Corrigan's,  454 
decurtate,  344 
feeling,  technic  of,  329 
gaseous,  339 
goat-leap,  343 
hyperdicrotic,  342 
hypertension  of,  339,  342 
hypotension  of,  339,  343 
in  aneurism  of  abdominal  aorta,  493 

of  thoracic  aorta,  486 
in  aortic  regurgitation,  454 

stenosis,  460 

in  croupous  pneumonia,  205 
in  edema  of  lungs,  189 
in  mitral  stenosis,  444 
in  pulmonary  regurgitation,  472 

stenosis,  468 
in  tricuspid  regurgitation,  464 

stenosis,  466 
intermission  of,  337 
irregularity  of,  337 
locomotive,  453 
Mouneret's,  339 
mouse-tail,  344 
movable,  453 
pistol,  454 
pressure,  33 
pulmonary,  437 
receding,  454 
rhythm  of,  329 
tension  of,  variations  in,  338 
velocity  of,  variations  in,  344 
venous,  346.     See  also  Venous  pulse. 
volume  of,  330 

variations,  343 
water-hammer,  454 
Pulse-rate,  329 

disturbances  of,  332 
Pulsus  alternans,  338,  370 

sphygmomanometer  in  study  of, 

36 
altus  et  celer  in  aortic  regurgitation, 

454 

anacrotic,  342 
bigeminus,  338 
bisferiens,  342 

in  aortic  stenosis,  460 
celer,  344 
celerity  of,  variations  in,  344 


582 


IXDKX 


Pulsus  celerrimus,  344 

in  aortic  regurgitation,  454 

deficiens,  338 

dicroticus,  342 

durus,  339 

equalis,  343 

frequens,  333 

inequalis,  343 
periodicus,  338 

intercidens,  338 

intermittens,  337 

irregularis  perpetuus,  369 

magnus,  343 

mollis,  339 

paradoxus,  338 

parvus,  343 

plenus,  343 

rarus,  336 

subungualis,  345 

tardus,  344 

in  aortic  stenosis,  460 

trigeminus,  338 

vacuus,  344 

Punctum  maximum  of  murmurs,  375 
Puncture,  47.  See  also  Paracentesis. 
Pupils,  inequality,  in  diseases  of  lungs 

and  pleura,  130 
Purulent  pericarditis,  401 

pleurisy,  278.     See  also  Empyema. 

pneumonia,  255 
Putrid  bronchitis,  175 
Pylorus,  clinical  anatomy,  519 
Pyopericardium,  401 
Pyopneumopericardium,  406 
Pyopneumothorax,  287 

subphrenic,  294 
Pyothorax,  278 


RACHITIC  rosary,  82 

thorax,  81 

Radial  sphygmogram,  330 
Radiography,  65 
Rales,  162 

atelectatic,  164 

bronchial,  162 

buccal,  162 

cardiopneumatic,  166 

cavernous,  162 

consonating,  207 

crepitant,  163 

dry,  162 

emphysematous,  163 

gurgling,  165 

hair,  161 

i  n<  lux.  164 

laryngeal,  162 
in  phthisis,  233 


Rales,  moist,  163 

mucous,  165 

redux,  164 
in  croupous  pneumonia,  206 

sibilant,  162 

sonorous,  162 

subcrepitant,  164 

subpleural,  168 

tracheal,  162 

vesicular,  162 
Rasmussen's  aneurism  in  chronic  ul- 

cerative  tuberculosis,  222 
Reaction,  atropin,  in  cardiac  compe- 
tency, 333 

Moro's,  69 

tuberculin,  67 
Receding  pulse  in  aortic  regurgitation, 

454 

Rectum,  clinical  anatomy,  534 
Recurrent  laryngeal  nerve  paralysis  in 

mitral  stenosis,  442 
Reflex,  lung,  151 
oculocardiac,  337 
renal,  559 

Reflexes,  vertebral,  22 
Regurgitation,  aortic,  449.     See  also 

Aortic  regurgitation. 
mitral,  434.     See  also  Mitral  regur- 
gitation. 
pulmonary,  471 

clinical  pathology,  471 
diagnosis,  473 
organic,  471 
physical  signs,  472 
pulse  in,  472 
relative,  472 
safety-valve,  435,  463 
tricuspid,  462.     See  also  Tricuspid 

regurgitation. 
Renal  asthma,  102 

reflex,  559 
Resistance,   increased,   in  diseases  of 

lungs  and  pleura,  134 
Resonance,  amphoric,  146 

band-box,  in  hypertrophic  emphy- 
sema of  lungs,  244 
cracked-pot,  147 
hydatid,  19 
impaired,  19 
jug,  147 

money-chink,  147 
osteal,  19 
pulmonary,  137 
.  anteriorly,  138 
exaggeration    of,    144.     See   also 

Hyperresonance,  pulmonary. 
extent  of,  140 
laterally,  138 


INDEX 


583 


Resonance,    pulmonary,    posteriorly, 

138 
regional  differences  in,  137 

Skodaic,  145 

vesicular,  137.      See  also  Resonance, 
pulmonary. 

vesiculotympanitic,  144 

vocal,  159 

Resonant  percussion-sounds,  13,  18 
Respiration,  92,  152 

abdominal,  93,  94 

absent,  158 

amphoric,  154 

anomalies  of,  95 

Biot's,  99 

bronchial,  153 

bronchocavernous,  154 

bronchovesicular,  152,  155 

cavernous,  154 

Cheyne-Stokes,  97 

cog-wheel,  158 

costal,  93,  95 

diaphragmatic,  93 

difficult,  loo.     See  also  Dyspnea. 

exaggerated,  156 

feeble,  157 

frequency,  alterations  in,  97 

harsh,  156 

prolonged,  156 

interrupted,  158 

irregularity,  97 

jerky,  97 

meningeal,  99 

normal,  92 

puerile,  156 

rapid,  97 

Seitz's  metamorphosing,  155 

senile,  157 

slow,  97 

sternomastoid,  95 

stertorous,  99 

stridulous,  99 

thoracic,  93 

type,  93 

reversal  of,  95 

vesicular,  152 

vesiculocavernous,  154 
Respiratory   alterations   of   subcostal 
angle,  94 

arhythmia,  97,  364 

cycle,  92 

movements  of  thorax,  92.     See  also 
Respiration. 

percussion,  136 

sounds,  152 

turgescence  of  cervical  veins,  1 29 
Retraction,  abnormal  areas  of,  324 
Rhonchal  fremitus,  134 


Rhonchus,  162 
Rhythm,  canter,  362 
gallop,  362 
nodal,  366,  369 
pendulum,  371 
Rib,    cervical,    pressure   of,    on    sub- 

clavian  artery,  492 
Ribs  as  landmarks  of  chest,  72,  73 
Riedel's  lobe,  545 
Robson's  point,  pain  at,  518 
Rod  auscultation,  16 
Rogers'Tnurmur,  475 
Rontgen  rays,  examination  by  means 

of,  65 

in  aneurism,  484 
in  chronic  interstitial  pneu- 
monia, 216 

in  croupous  pneumonia,  205 
in  gall-stones,  542 
in  gastric  cancer,  525 
diseases,  524 
ulcer,  525 
in  mediastinal  lymphadenitis, 

301 

neoplasm,  307 
in  phthisis,  228 
in  pleural  effusion,  271 
in  pneumothorax,  290 
of  large  intestine,  534 
Rosary,  rachitic,  82 
Rotch's  sign,  400 
Rothschild's  sign  in  phthisis,  224 
Ruptured  compensation  of  heart,  431 


SABOURIN'S  sign  of  apical  phthisis,  226 
Saccular  aneurism  of  thoracic  aorta, 

477 
Sacral  region,  pain  in,  120 

triangle,  497 
Sacrum,  pain  in,  519 
Safety-valve  murmur,  378 

regurgitation,  435,  463 
Sahli's  theory  of  vesicular  breathing, 

153 

Sander's  sign,  404 
Sansom's  double  shock  sound,  445 

leaden  overcast,  316 

sign  in  aneurism  of  thoracic  aorta, 
488 

stethoscope,  25 
Sarcoma  of  lungs,  263 

of  pleura,  296 
Scaphoid  abdomen,  504 

scapula,  73 
Scapula,  alar,  78 

scaphoid,  73 

winged,  78 


IXDKX 


Scapular  line,  74 
spinal,  77 

region,  77 
Scars  of  thorax,  121 

on  skin  of  abdomen,  514 
Schusterbrust,  84 
Sclerosis  of  lung,  213 
Scoliosis,  82 

Scorbiculus  cordis,  7 1 ,  496 
See-saw  murmur  in  aortic  regurgita- 

tion,  456 
Seitz's    metamorphosing    respiration, 

iSS 

Semilunar  space,  Traube's,  530 
Senile  atrophy  of  lungs,  246 

respiration,  157 

Septum,  absence  of,  between  auricles 
and  ventricles,  474 

interventricular,    defects    of,    473, 

475 
Serofibrinous    pericarditis,    398.     See 

also  Pericarditis,  serofibrinous. 
pleurisy,  268 

Bacelli's  sign  in,  275 
clinical  pathology,  268 
diagnosis,  276 
Ellis'  line  in,  273 
Grocco's  sign  in,  273 
physical  signs,  270 
Serum  illness,  52 
Shoulder,  pain  in,  117 
Shoulder-blade  friction,  168 
Shoulder-joint  friction,  168 
Shulman's  sign,  511 
Sibilant  rales,  162 
Sibson's  furrow,  73 

notch,  400 
Siderosis,  252 

Sigmoid  flexure,  clinical  anatomy,  534 
Sign,  Auenbrugger's,  399 
Bacelli's,  160,  275 
Bassler's,  537 
Bastedo's,  537 
Biermer's,  150 
Broadbent's,  324,  404 
Bryson's,  96 
Drummond's,  488 
Duroziez's,  394,  457 
Erni's,  231 
d'Espine's,  300 
Ewart's,  399       ^ 
Friedreich's,  147,  323,  404 
Gerhardt's,  150 
Glasgow's,  488 
Grocco's,  143,  273 
Jiirgensen's,  219 
Kussmaul's,  326,  404 
Litten's,  93 


Sign,  Lombardi's,  226 

Lorenz's,  224 

Mussel's,  452 

Naunyn's,  518 

Oliver's,  328 

Perez's,  168 

Rotch's,  400 

Rothschild's,  224 

Sabourin's,  226 

Sander's,  404 

Sansom's,  488 

Shulman's,  511 

Skoda's,  145 

Stiller's,  527 

Traube's,  457 

Turrettini's,  398 

Williams',  227 

Wintrich's,  148 
Signe  du  sou,  151 

du  tapotage,  231 
Sino-auricular  node  of  Keith  and  Flack, 

.313 

Sinus  arhythmia,  364 
Situs  viscerum  inversus,  474 
Skin  of  abdomen,  513 
Skodaic  resonance,  145 
Slow  consumption,  220 
Smith's  murmur  in  mediastinal  lym- 
phadenitis, 301 
Snoring,  99 

Soft-valve  mitral  stenosis,  441 
Sonorous  rales,  162 
Souffle.     See  Bruit. 
Sounds,  adventitious,  160 

cardiac,  356.   See  also  Heart-sounds. 

extraneous,  161 

falling-drop,  170 

Huchard's  percussion,  190 

intestinal,  503 

metallic,  170 

muscle,  161 

pulmonary  fistula,  165 

respiratory,  152 

splashing,  169 

stomach,  503 

succussion,  169 
Hippocratic,  170 
of  stomach,  527 
Spasm,  lumbar  muscle,  559 
Spasmodic  asthma,  177 
Spens'  syndrome,  368 
Sphacelation,  pulmonary,  257 
Sphygmocardiogram,  interpretation  of, 

40 

Sphygmocarciograph,  Jacquet's,  38 
Sphygmocardiography,   clinical   value 
of,  42 

technic  of,  37 


INDEX 


Sphygmogram,  arterial,  40,  330 

clinical  significance,  330 

radial,  330 

venous,  42 

Sphygmograph,  Dudgeon's,  39 
Sphygmography,  37 
Sphygmomanometer,  Hill-Barnard,  34 

in  study  of  pulsus  alternans,  36 

Nicholson's,  31 

Rogers',  33 
Sphygmomanometry,  31 

auscultatory  method,  33 

technic,  31 
Spinal  percussion,  20 

scapular  line,  77 

zones,  Koranyi's,  21 
Spine,  iliac,  anterior  superior,  496 

pubic,  496 

Splashing  sounds,  169 
Spleen,  auscultation  of,  556 

clinical  anatomy,  550 

displacement  of,  553 

enlargements  of,  553 

examination  of,  550 

inspection  of,  551 

pain  in  region  of,  553 

palpation  of,  551 

percussion  of,  554 

Point,  553 

pulsations  of,  553 

puncture  of,  exploratory,  64 

tenderness  in  region  of,  553 
Splenic  flexure,  clinical  anatomy,  534 

friction-sound,  556 

systolic  bruit,  556 
Splenization,  pulmonary,  187 
Splenoptosis,  554 

Sputum  in  croupous  pneumonia,  204 
Stenosis,  aortic,  457.     See  also  Aortic 
stenosis. 

funnel-shaped,  mitral,  440 

mitral,  439.     See  also  Mitral  stenosis. 

of  bronchi,  183 

of  upper  air-passages  as  cause  of 
dyspnea,  102 

pulmonary,  467 
congenital,  473 
clinical  pathology,  467 
diagnosis  of,  469 
physical  signs,  468 
pulse  in,  468 
relative,  468 

soft- valve,  mitral,  441 

subaortic,  459 

tricuspid,  465.     See  also  Tricuspid 

stenosis. 
Sternal  dulness,  143 

line,  74 


Sternal  pain,  117 

region,  77 

thrill  over,  328 
Sternomastoid  breathing,  95 
Sternum  as  landmark  of  thorax,  71 

enlargement  of  veins  about,  105 
Stertorous  respiration,  99 
Stethoscope,  Arnold's,  26 

binaural,  24 

Bowies',  24 

choice,  23 

differential,  26 

double,  24 

Hawksley's,  26 

monaural,  24 

Sansom's,  25 

single,  24 
Stiller 's  sign,  527 
Stokes-Adams'  bradycardia,  369 
Stone-cutter's  phthisis,  252 
Stomach,  auscultation  of,  531 

auscultatory  percussion  of,  530 

body  of,  clinical  anatomy,  5  20 

canal  of,  clinical  anatomy,  520 

cancer  of,  pain  in,  526 
x-ray  examination  in,  5  25 

clinical  anatomy,  519 

contents,  effervescence  of,  531 

deglutition  murmur  of,  531 

examination  of,  519 

fundus  of,  clinical  anatomy,  520 

greater  curvature  of,  clinical  anat- 
omy, 521 

gurgling  in,  531 

hour-glass,  523 

incisura  angularis  of,  clinical  anat- 
omy, 521 

inspection  of,  521 

lesser  curvature  of,  clinical  anatomy, 
520 

mechanical  inflation,  522 

pain  in,  5  26 

palpation  of,  525 

percussion  of,  529 

perforation  of,  metallic  rub  in,  531 

peristalsis  of,  512 

sounds,  503 

stroke  auscultation  of,  531 

succussion  sounds  of,  527 

transillumination  of,  525 

tumors  of,  pain  in,  526 

tympany  of,  decrease,  531 
increase,  531 

ulcer  of,  pain  of,  526 

*-ray  examination  in,  525 

vestibule  of,  clinical  anatomy,  520 

x-ray  examination,  524 
Stomach-tube,  use  of,  527 


INDEX 


Striae  vasculares  in  chronic  ulcerative 

phthisis,  226 
Stridor  serraticus,  100 
Stridulous  respiration,  99 
String  galvanometer,  Lewis'  diagram 

of,  45 

Stripe  pneumonia,  199 
Stroke  auscultation,  16 

of  stomach,  531 
Subaortic  stenosis,  459 
Subclavian  artery,  aneurism  of,  490 
pressure  of  cervical  rib  on,  492 
Subcostal  angle,  73 

respiratory  alterations  of,  94 
Subcrepitant  rales,  164 
Subcrepitations,  atelectatic,  165 
Subcutaneous  nodules  of  abdomen,  514 

tissue  of  abdomen,  513 
Submaxillary  glands,  enlargement,  no 
Subphrenic  pyopneumothorax,  294 
Subpleural  crepitation,  168 
Succussio    Hippocratis    in    pneumo- 

thorax,  292 

Succussion  fremitus,  134 
sounds,  169 

Hippocratic,  170 
of  stomach,  527 
pericardial,  392 
Suffocative  catarrh,  192,  195 
Suffusion,  venous,  of  neck,  129 
Sulcus,  Harrison's,  83 
Suppurative   mediastinal   lymphaden- 
itis, 298 

mediastinitis,  297 
Supracardiac    vascular    area,    clinical 

anatomy,  310 
Supraclavicular  region,  77 
Suprascapular  region,  77 
Symphysis  pleurae,  283 

pubis,  496 

Syndrome,  Spens',  368 
Stokes- Adams',  368 
Syphilis,  pulmonary,  237 
acquired,  238 
clinical  pathology,  237 
congenital,  238 
diagnosis,  239 
physical  signs,  239 
Syphilitic  pneumonia,  237 
Systole,  auricular,  313 

ventricular,  314 
Systolic  bruit  over  spleen,  556 
epigastric  throbbing,  324 
murmurs,  374 
aortic,  383 
apical,  378 
arterial,  392 
mitral,  383 


Systolic  murmurs,  pulmonic,  378,  387 

tricuspid,  378,  385 
plateau,  42,  320 
souffle  over  gall-bladder,  549 
venous  pulse,  348 


TACHYCARDIA,  333 

auricular,  334 

paroxysmal,  336 
Tactile  friction  of  abdomen,  516 
Tawara's  node,  313 
Test,  Calmette's,  68 

Gairdner's,  147 

Koch's  tuberculin,  67 

von  Pirquet's,  67 

Thoracic  aorta,  aneurism  of,  476.     See 
also  Aneurism  of  thoracic  aorta. 

glands,  lateral,  enlargement  of,  114 

index,  Fourmentin's,  70 

respiration,  93 

vertebra,  twelfth  line  of,  77 
Thoracometry,  29 
Thorax,  alar,  78 

anterior,  percussion  of,  135 

asymmetry  of,  86 

barrel-,  78,  79 

boat-shaped,  86 

clavicles  as  landmarks  of,  72 

clinical  anatomy,  70 

depressions  of,  local,  90 

edema  of,  106 

emphysematous,  78 

en  bateau,  86 

en  gouttiere,  86 

examination  of,  70 

expansion  of,  alterations  in  degree,  95 
deficiency  in,  95 
Bryson's  sign,  96 
circumscribed,  96 
increase  in,  96 
unsymmetric,  96 
wavy  and  uneven,  96 

expiratory  form,  78 

flat,  84 

fusiform,  85 

glandular  enlargements,  109 

gutter-,  86 

inflated,  78 

inspiratory  form,  80 

intercostal  spaces  as  landmarks  of, 
72 

lateral  regions,  percussion  of,  136 
wall,  pain  in,  119 

lower,  enlargement  of  veins  of,  106 

mensuration  of,  29 

movements  of,   mechanical  restric- 
tion, as  cause  of  dyspnea,  103 


INDEX 


Thorax,  nipple  as  landmark  of,  .73 

normal  landmarks,  71 

of  atrophic  emphysema,  80 

of  progressive  muscular  atrophy,  86 

pain  in,  117 

paralytic,  78 

pathologic  types,  77 

phthisical,  78 

posterior  wall,  pain  in,  119 

prominences  of,  circumscribed,  89 

pterygoid,  78 

rachitic,  81 

respiratory  movements,  92.     See  also 
Respiration. 

ribs  as  landmarks  of,  72,  73 

scars  of,  121 

sternum  as  landmark,  71 

topographic  lines  and  areas,  74 

unilateral  bulging,  86 
contraction,  88 

upper,  ramification  of  small  venules 
over,  105 

venous  enlargement  and  tortuosity 
over,  104 

vertical  measurement,  70 
Threshold   percussion,    Goldscheider's 

meth"od,  14 
Thrill,  327 

abdominal,  516 

at  apex  of  heart,  327 

at  base  of  heart,  327 

at  intercostal  spaces,  327 

hydatid,  516 

over  sternal  region,  328 

over  xiphoid  region,  328 

palpable,  in  epigastrium,  516 
Thymus  gland,  movable  dulness  of,  492 
Thyroid  gland,  enlargement,  116 
Tinkling,  metallic,  170 
Tortuous    and    enlarged    veins    over 

abdomen,  514 
Toxemic  dyspnea,  101 
Toxic  pneumonia,  208 
Trachea,  clinical  anatomy,  1 26 

rales,  162 

tone,  Williams',  149 

tugging,  328 

Tracheobronchitis,  acute,  171 
Transudate  in  pleural  fluid,  53 
Traube's  plugs  in  fetid  bronchitis,  175 

semilunar  space,  530 

sign  in  aortic  regurgitation,  457 

space,  dulness  of  normal  tympany 

in,  143 

Traumatic  pneumonia,  210 
Triangle,  sacral,  497 
Trichertbrust,  83 
Tricuspid  area,  356 


Tricuspid  murmurs,  385 
presystolic,  385 
systolic,  378,  385 
regurgitation,  462 

clinical  pathology,  462 
diagnosis,  465 
organic,  462 
physical  signs,  463 
pulse  in,  464 
relative,  463 
stenosis,  465 

clinical  pathology,  465 
diagnosis,  467 
physical  signs,  466 
pulse  in,  466 

valve,  clinical  anatomy,  310 
True  aneurism  of  thoracic  aorta,  478 
Trypanosome  gambiense  in    cerebro- 

spinal  fluid,  64 
Tubercle  friction,  503 

in  tuberculous  peritonitis,  516 
Tuberculin  reaction,  67 
test,  Calmette's,  68 
Koch's,  67 
von  Pirquet's,  67 
Tuberculofibrosis  of  lungs,  234 
Tuberculosis,  chronic  ulcerative,  Ras- 

mussen's  aneurism  in,  222 
of  bronchial  glands,  299 
Tugging,  tracheal,  328 
Tumors  of  mediastinum,  301 
clinical  pathology,  301 
diagnosis,  307 
physical  signs,  302 
of  pleura,  295 
of  stomach,  pain  in,  526 
pulmonary,  260 
Tuning-fork  auscultation,  28 
Turrettini's  sign,  398 
Tussile  fremitus,  134 
Tympanic  percussion-sounds,  13,  19 
Tympanites,  pulmonary,  145 
Tympany,  bell,  150 

from   parabronchial   consolidations, 

146 
gastric,  decrease  of,  531 

increase  of,  531 
in  bronchiectatic  cavities,  145 
in  pneumothorax,  146 
in  pulmonary  cavities,  145 
pulmonary,  144 

acute,  145 
Typhoid  pneumonia,  208 


ULCER,  gastric,  pain  of,  526 

z-ray  examination  in,  525 
Ulcerative  endocarditis,  423 


IXDKX 


Ulcerative  phthisis,  chronic,  220.    See 
also  Phthisis,  chronic  ulcerative. 

Ulceres  du  poumon,  255 

Umbilical  changes,  514 
notch,  539 
region,  499 
pain  in,  518 

Umbilicus,  497 

Uremic  dyspnea,  101 


VALVES,  aortic,  310 
areas,  310 

of  heart,  356 

beaded  excrescences  of,  423 
ileocecal,  533 
mitral,  310 
of  heart,  310 
polypous  lesions  of,  423 
pulmonic,  310 
tricuspid,  310 

verrucose  excrescences  of,  423 
villous  lesions  of,  423 
Valvular  disease,  chronic,  427 
Valvulitis,  421 
Varicose  aneurism,  479 
Varix,  aneurismal,  478 
Vascular  dulness,  area  of,  352 

murmurs,  392 
Veiled  puff,  Laennec's,  155 
Veines  fluides,  373 
Veins,  cervical,  respiratory,  turgescence, 

129 

engorgement  of,  326 
enlarged  and  tortuous,  over  abdo- 
men, 514 

enlargement  of,  about  sternum,  105 
of  costal  arch,  106 
of  lower  thorax,  106 
of  upper  arm,  105 
over  thorax,  104 
fluid,  373 

innominate,  clinical  anatomy,  311 
jugular,  diastolic  collapse,  323 
engorgement  of,  326 
pulsations  of,  322 
mammary,  enlarged,  105 
ramification  of,  over  upper  chest,  105 
tortuosity  of,  over  thorax,  104 
Vena  cava,  inferior,  clinical  anatomy, 

497 
superior  aneurism  of,  490 

clinical  anatomy,  311 
Venous   blood-pressure,    instrumental 

estimation,  36 

Oliver's  method  of  estimating,  36 
bruit,  hepatic,  549 
engorgement,  325 


Venous  flow,  direction  of,  105 
hum,  394 
pulse,  346 

auricular,  347 

in  aortic  regurgitation,  435 

penetrating,  349 

physiologic,  42 

ventricular,  348 
sphygmogram,  42 
suffusion  of  neck,  129 
Ventricular  diastole,  314 
extrasystoles,  365 
fibrillation,  370 
systole,  314 
Vermiform  appendix,  clinical  anatomy, 

533 

VerneuiPs  pseudolipoma,  90 
Verrucose  excrescences  of  valves,  423 
Vertebra,    twelfth    thoracic,    line    of, 

77 

Vertebral  reflexes,  22 
Vesicular  emphysema,  240.     See  also 
Emphysema,  pulmonary. 

rales,  162 

resonance,  137.     See  also  Resonance, 
pulmonary. 

respiration,  152 

Vesiculocavernous  respiration,  154 
Vesiculotympanitic  resonance,  144 
Vesiculotympany  in  hypertrophic 

emphysema  of  lungs,  244 
Vicarious  emphysema  of  lungs,  246 
Villous  lesions  of  valves,  423 
Viscera,   abdominal,   examination   of, 

495 

topographic  lines  and  areas,  498 
Visceral  paracentesis,  64 

pleura,  127 
Vocal  fremitus,  131 

resonance,  159 
Voice  fremitus,  influence  of  decubitus 

on, 132 

Voillemier's  point,  519 
von  Pirquet's  tuberculin  test,  67 


WAIST,  wasp,  86 

Wandering  pneumonia,  199 

Wassermann  reaction  in  cerebrospinal 
fluid,  64 

Water-hammer  pulse  in  aortic  regur- 
gitation, 454 

Water-whistle  noise,  165 
in  pneumothorax,  292 

Whispering  pectoriloquy,  159 

White  hepatization  of  lung,  237 
pneumonia,  237 
of  fetus,  237 


INDEX 


589 


Williams'  sign  in  phthisis,  227 

tracheal  tone,  149 
Winged  scapulae,  78 
Winter  cough,  146 

Wintrich's  interrupted  change  of  note, 
148 

sign,  148 
WoUlez's  disease,  186 


XIPHISTERNAL  crunching,  358 

joint,  71 
Xiphoid  crepitation,  516 

region,  thrill  over,  328 
X-ra.ys.     See  Rontgen  rays. 

ZAGOUMENNY'S  rule,  53 
Zones,  spinal  percussion,  21 


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subjected  his  book  to  a  most  thorough  revision.  Many  new  subjects  have  been 
added,  a  number  in  the  former  edition  have  been  rewritten,  and  throughout  the 
book  reference  has  been  made  to  vaccine  and  serum  therapy,  to  the  relation  of 
tuberculosis  to  ocular  disease,  and  to  the  value  of  tuberculin  as  a  diagnostic  and 
therapeutic  agent. 

The  text  is  fully  illustrated  with  black  and  white  cuts  and  colored  plates,  and 
is.  every  way  the  book  maintains  its  reputation  as  an  authority  upon  the  eye. 


PERSONAL  AND   PRESS  OPINIONS 


Samuel  Theobald,  M.D 

Clinical  Professor  of  Ophthalmology,  Johns  Hopkins  University,  Baltimore. 
"  It  is  a  work  that  I  have  held  in  high  esteem,  and  is  one  of  the  two  or  three  books  upon 
the  eye  which  I  have  been  in  the  habit  of  recommending  to  my  students  in  the  Johns  Hopkins 
Medical  School." 

University  of  Pennsylvania  Medical  Bulletin 

"  Upon  reading  through  the  contents  of  this  book  we  are  impressed  by  tne  remarkable 
fulness  with  which  it  reflects  the  notable  contributions  recently  made  to  ophthalmic  literature. 
No  important  subject  within  its  province  has  been  neglected." 

Johns  Hopkins  Hospital  Bulletin 

'  No  single  chapter  can  be  selected  as  the  best.  They  are  all  the  product  of  a  finished 
authorship  and  the  work  of  an  exceptional  ophthalmologist.  The  work  is  certainly  one  of  the 
best  on  ophthalmology  extant,  and  probably  the  best  by  an  American  author." 


SAUNDERS'  BOOKS   ON 


GET  Jk  •  THE  NEW 

THE    BEST  t\  111  6  r  1  C  &  II  STANDARD 

Illustrated   Dictionary 

New  (?th)  Edition— 5000  Sold  in  Two  Months 


The  American  Illustrated  Medical  Dictionary.  A  new  and  com- 
plete dictionary  of  the  terms  used  in  Medicine,  Surgery,  Dentistry, 
Pharmacy,  Chemistry,  Veterinary  Science,  Nursing,  and  kindred 
branches ;  with  over  100  new  and  elaborate  tables  and  many  illustra- 
tions. By  W.  A.  NEWMAN  BORLAND,  M.D.,  Editor  of  "  The  American 
Pocket  Medical  Dictionary."  Large  octavo,  with  1107  pages,  bound  in 
full  flexible  leather.  Price,  $4.50  net;  with  thumb  index,  $5.00  net. 

KEY  TO  CAPITALIZATION  AND  PRONUNCIATION— ALL  THE  NEW  WORDS 

This  dictionary  is  the  "new  standard."  It  defines  hundreds  of  the  newest 
terms  not  defined  in  any  other  dictionary — bar  none.  These  terms  are  live, 
active  words,  taken  right  from  modern  medical  literature. 

Howard  A.  Kelly.  M.  l>., 

Professor  of  Gynecologic  Surgery,  Johns  Hopkins  University,  Baltimore 
"  Dr.  Dorland's  Dictionary  is  admirable.     It  is  so  well  gotten  up  and  of  such  convenient 
size.     No  errors  have  been  found  in  my  use  of  it." 

Theobald's  Prevalent  Eye  Diseases 


Prevalent  Diseases  of  the  Eye.  By  SAMUEL  THEOBALD,  M.  D., 
Clinical  Professor  of  Ophthalmology  and  Otology,  Johns  Hopkins 
University.  Octavo  of  5 50  pages,  with  2 19  text-cuts  and  several  colored 
plates.  Cloth,  $4.50  net ;  Half  Morocco,  $6.00  net. 

THE    PRACTITIONER'S    OPHTHALMOLOGY 

With  few  exceptions  all  the  works  on  diseases  of  the  eye,  although  written 
ostensibly  for  the  general  practitioner,  are  in  reality  adapted  only  to  the  specialist ; 
but  Dr.  Theobald  in  his  book  has  described  very  clearly  and  in  detail  those  condi- 
tions, the  diagnosis  and  treatment  of  which  come  within  the  province  of  the  general 
practitioner.  The  therapeutic  suggestions  are  concise,  unequivocal,  and  specific. 
It  is  the  one  work  on  the  Eye  written  particularly  for  the  general  practitioner. 

Charles  A.  Oliver,  M.D.. 

Clinical  Professor  of  Ophthalmology,  Woman's  Medical  College  of  Pennsylvania. 

"  I  feel  I  can  conscientiously  recommend  it,  not  only  to  the  general  physician  and  medical 
student,  for  whom  it  is  primarily  written,  but  also  to  the  experienced  ophthalmologist.  Most 
•urely  Dr.  Theobald  has  accomplished  his  purpose." 


DISEASES   OF   THE  EYE. 


Haab  and  DeSchweinitz's 
External  Diseases  of  the  Eye 

Atlas  and  Epitome  of  External  Diseases  of  the  Eye.     By  DR.  O. 

HAAB,  of  Zurich.  Edited,  with  additions,  by  G.  E.  DESCHWEINITZ, 
M.  D.,  Professor  of  Ophthalmology,  University  of  Pennsylvania.  With 
101  colored  illustrations  on  46  lithographic  plates  and  244  pages  of 
text.  Cloth,  $3.00  net.  In  Saunders'  Hand-Atlas  Series. 

THE  NEW   (3d)    EDITION 

Conditions  attending  diseases  of  the  external  eye,  which  are  often  so  complicated, 
have  probably  never  been  more  clearly  and  comprehensively  expounded  than  in 
the  forelying  work,  in  which  the  pictorial  most  happily  supplements  the  verbal 
description.  The  price  of  the  book  is  remarkably  low. 

The  Medical  Record,  New  York 

"  The  work  is  excellently  suited  to  the  student  of  ophthalmology  and  to  the  practising 
physician.     It  cannot  fail  to  attain  a  well-deserved  popularity." 

Haab  and  DeSchweinitzV 
Ophthalmoscopy 


Atlas  and  Epitome  of  Ophthalmoscopy  and  Ophthalmoscopic 
Diagnosis.  By  Dr.  O.  HAAB,  of  Zurich.  Edited,  with  additions,  by 
G.  E.  DESCHWEINITZ,  M.  D.,  Professor  of  Ophthalmology,  University 
of  Pennsylvania.  With  152  colored  lithographic  illustrations  and  92 
pages  of  text.  Cloth,  $3.00  net.  In  Saunders'  Hand-Atlas  Series. 

THE  NEW   (2d)    EDITION 

The  great  value  of  Prof.  Haab's  Atlas  of  Ophthalmoscopy  and  Ophthalmo- 
scopic Diagnosis  has  been  fully  established  and  entirely  justified  an  English 
translation.  Not  only  is  the  student  made  acquainted  with  carefully  prepared 
ophthalmoscopic  drawings  done  into  well-executed  lithographs  of  the  most  im- 
portant fundus  changes,  but,  in  many  instances,  plates  of  the  microscopic  lesions 
are  added.  The  whole  furnishes  a  manual  of  the  greatest  possible  service. 

The  Lancet,  London 

"We  recommend  it  as  a  work  that  should  be  in  the  ophthalmic  wards  or  in  the  library  of 
every  hospital  into  which  ophthalmic  cases  are  received." 


SAUNDERS'  BOOKS  ON 


Cradle's 
Nose,  Pharynx*  and  Ear 

Diseases  of  the  Nose,  Pharynx,  and  Ear.  By  HENRY  GRADLE, 
M.D.,  late  Professor  of  Ophthalmology  and  Otology,  Northwestern 
University  Medical  School,  Chicago.  Octavo  of  547  pages,  illustrated, 
including  two  full-page  plates  in  colors.  Cloth,  $3.50  net. 

INCLUDING  TOPOGRAPHIC  ANATOMY 

This  volume  presents  diseases  of  the  Nose,  Pharynx,  and  Ear  as  the  author 
has  seen  them  during  an  experience  of  nearly  twenty-five  years.  In  it  are 
answered  in  detail  those  questions  regarding  the  course  and  outcome  of  diseases 
which  cause  the  less  experienced  observer  the  most  anxiety  in  an  individual  case. 
Topographic  anatomy  has  been  accorded  liberal  space. 

Pennsylvania  Medical  Journal 

"This  is  the  most  practical  volume  on  the  nose,  pharynx,  and  ear  that  has  appeared 
recently.  ...  It  is  exactly  what  the  less  experienced  observer  needs,  as  it  avoids  the  confusion 
incident  to  a  categorical  statement  of  everybody's  opinion." 

Kyle's 
Diseases  of  Nose  am)  Throat 


Diseases  of  the  Noae  and  Throat.  By  D.  BRADEN  KYLE,  M.  D.? 
Professor  of  Laryngology  in  the  Jefferson  Medical  College,  Phila- 
delphia. Octavo,  825  pages;  with  258  illustrations,  28  in  colors. 
Cloth,  $4.50  net;  Half  Morocco,  £6.00  net. 

JUST  OUT— THE  NEW  (5th)  EDITION 

The  new  (jM)  edition  of  Dr.  Kyle's  work  shows  an  inc reuse  of  TOO  pages  and 
some  40  new  illustrations.  The  following  new  articles  have  been  added :  vaccine 
therapy  ;  lactic  bacteriotherapy;  salvarsan  in  the  treatment  of  syphilis  of  the  upper 
respiratory  tract ;  sphenopalatine  ganglia  neuralgia  ;  negative  air-pressure  in  ac- 
cessory sinus  disease  ;  chronic  hyperplastic  ethmoiditis  ;  and  congenital  insuffi- 
ciency of  the  palate.  The  tables  of  differential  diagnosis  and  the  prescriptions  are 
striking  points  of  Ur.  Kyle's  book. 

Pennsylvania  Medical  Journal 

"  Dr.  Kyle's  crisp,  terse  diction  has  enabled  the  inclusion  of  all  needful  nose  and  throat 
knowledge  in  this  book'." 


URINE  AND   IMPOTENCE. 


Ogden  on  the  Urine 


Clinical  Examination  of  Urine  and  Urinary  Diagnosis.  A  Clinical 
Guide  for  the  Use  of  Practitioners  and  Students  of  Medicine  and  Sur- 
gery. By  J.  BERGEN  OGDEN,  M.  D.,  Medical  Chemist  to  the  Metro- 
politan Life  Insurance  Company,  New  York.  Octavo,  418  pages,  54 
text  illustrations,  and  a  number  of  colored  plates.  Cloth,  $3.00  net. 

THE  NEW  (3d)  EDITION 

In  this  edition  the  work  has  been  brought  absolutely  down  to  the  present  day. 
Urinary  examinations  for  purposes  of  life  insurance  have  been  incorporated,  because, 
a  large  number  of  practitioners  are  often  called  upon  to  make  such  analyses. 
Special  attention  has  been  paid  to  diagnosis  by  the  character  of  the  urine,  the 
diagnosis  of  diseases  of  the  kidneys  and  urinary  passages  ;  an  enumeration  of  the 
prominent  clinical  symptoms  of  each  disease  ;  and  the  peculiarities  of  the  urine 
in  certain  general  diseases. 

The  Lancet,  London 

"  We  consider  this  manual  to  have  been  well  compiled  ;  and  the  author's  own  experience, 
so  clearly  stated,  renders  the  volume  a  useful  one  both  for  study  and  reference." 

Pilcher's 
Practical  Cystoscopy 

Practical  Cystoscopy.  By  PAUL  M.  PILCHER,  M.  D.,  Consulting 
Surgeon  to  the  Eastern  Long  Island  Hospital.  Octavo  of  398  pages, 
with  233  illustrations,  29  in  colors.  Cloth,  $5.50  net. 

DIAGNOSIS  AND  TREATMENT 

Cystoscopy  is  to-day  the  most  practical  manner  of  diagnosing  and  treating 
diseases  of  the  bladder,  ureters,  kidneys,  and  prostate.  To  be  properly  equipped, 
therefore,  you  must  have  at  your  instant  command  the  information  this  book  gives 
you.  It  explains  away  all  difficulty,  telling  you  why  you  do  not  see  something 
when  something  is  there  to  see,  and  telling  you  how  to  see  it.  All  theory  has 
been  uncompromisingly  eliminated,  devoting  every  line  to  practical,  needed- 
every-day  facts,  telling  you  how  and  when  to  use  the  cystoscope  and  catheter — 
telling  you  in  a  way  to  make  you  know.  The  work  is  complete  in  every  detail. 

Bransford  Lewis,  M.  D.,  St.  Louis  University. 

"  I  am  very  much  pleased  with  Dr.  Pilcher's  '  Practical  Cystoscopy.'     I  think  it  is  the  best 

in  the  English  language  now."— April  27, 


lo  SAUNDERST   BOOKS    ON 

Goepp's 
Dental   State   Boards 

Dental  State  Board  Questions  and  Answers By  R.  MAX  GOEPP, 

M.  D.,  author  "  Medical  State  Board  Questions  and  Answers."  Octavo 
of  428  pages.  Cloth,  $2.75  net. 

COMPLETE  AND  ACCURATE 

This  new  work  is  along  the  same  practical  lines  as  Dr.  Goepp's  successful  work 
on  Medical  State  Boards.  The  questions  included  have  been  gathered  from  reliable 
sources,  and  embrace  all  those  likely  to  be  asked  in  any  State  Board  examination 
in  any  State.  They  have  been  arranged  and  classified  in  a  way  that  makes  for  a 
rapid  resume  of  every  branch  of  dental  practice,  and  the  answers  are  couched  in 
language  unusually  explicit — concise,  definite,  accurate. 

The  practicing  dentist,  also,  will  find  here  a  work  of  great  value — a  work 
covering  the  entire  range  of  dentistry  and  extremely  well  adapted  for  quick 
reference. 

Haab  and  deSchweinitz's 
Operative  Ophthalmology 

Atlas  and  Epitome  of   Operative    Ophthalmology.       By  DR.  O. 

HAAB,  of  Zurich.  Edited,  with  additions,  by  G.  E.  DE  SCHWEINITZ, 
M.  D.,  Professor  of  Ophthalmology  in  the  University  of  Pennsylvania. 
With  30  colored  lithographic  plates,  154  text-cuts,  and  375  pages  of 
text  /«  Sounders'  Hand-Atlas  Series.  Cloth,  $3.50  net. 


Dr.  Haab's  Atlas  of  Operative  Ophthalmology  will  be  found  as  beautiful  and 
as  practical  as  his  two  former  atlases.  The  work  represents  the  author' s  thirty 
years'  experience  in  eye  work.  The  various  operative  interventions  are  described 
with  all  the  precision  and  clearness  that  such  an  experience  brings.  Recognizing 
the  fact  that  mere  verbal  descriptions  are  frequently  insufficient  to  give  a  clear 
idea  of  operative  procedures,  Dr.  Haab  has  taken  particular  care  to  illustrate 
plainly  the  different  parts  of  the  operations. 

Johns  Hopkins  Hospital  Bulletin 

"  The  descriptions  of  the  various  operations  are  so  clear  and  full  that  the  volume  can  well 
hold  place  with  more  pretentious  text-books." 


GENITO-URINARY  AND    NOSE,     THROAT,    ETC.  11 

Greene  and  Brooks' 
Genito-Urinary  Diseases 

Diseases  of    the   Genito-Urinary  Organs  and  the  Kidney.      By 

ROBERT  H.  GREENE,  M.  D.,  Professor  of  Genito-Urinary  Surgery  at 
Fordham  University;  and  HARLOW  BROOKS,  M.  D.,  Assistant  Pro- 
fessor of  Clinical  Medicine,  University  and  Bellevue  Hospital  Medical 
School.  Octavo  of  639  pages,  illustrated.  Cloth,  $5.00  net;  Half 
Morocco,  $6.50  net. 

THE  NEW   (3d)  EDITION 

This  new  work  presents  both  the  medical  and  surgical  sides.  Designed  as  a 
work  of  quick  reference,  it  has  been  written  in  a  clear,  condensed  style,  so  that 
the  information  can  be  readily  grasped  and  retained.  Kidney  diseases  are  very 
elaborately  detailed. 

New  York  Medical  Journal 

"  As  a  whole  the  book  is  one  of  the  most  satisfactory  and  useful  works  on  genito-urinary 
diseases  now  extant,  and  will  undoubtedly  be  popular  among  practitioners  and  students." 

Gleason  on  Nose,  Throat, 
and  Ear 

A   Manual   of   Diseases  of   the   Nose,  Throat,  and    Ear.     By  E. 

BALDWIN  GLEASON,  M.  D.,  LL.  D.,  Professor  of  Otology,  Medico- 
Chirurgical  College,  Philadelphia.  I2mo  of  590  pages,  profusely  illus- 
trated. Cloth,  $2.50  net. 

JUST  OUT— THE  NEW  (3d)  EDITION 

Methods  of  treatment  have  been  simplified  as  much  as  possible,  so  that  in 
most  instances  only  those  methods,  drugs,  and  operations  have  been  advised 
which  have  proved  beneficial.  A  valuable  feature  consists  of  the  collection  of 
formulas. 

American  Journal  of  the  Medical  Sciences 

"  For  the  practitioner  who  wishes  a  reliable  guide  in  laryngology  and  otology  there  are  few 
books  which  can  be  more  heartily  commended." 


American  Text-Book  of  Genito-Urinary  Diseases,  Syphilis,  and 
Diseases  of  the  Skin.  Edited  by  L.  BOLTON  BANGS,  M.  D.,  and 
W.  A.  HARDAWAY,  M.  D.  Octavo,  1229  pages,  300  engravings,  20 
colored  plates.  Cloth,  $7.00  net. 


12  SAUNDERS*  BOOKS  ON 

Holland's  Medical 
Chemistry  and  Toxicology 

A  Text-Book  of  Medical  Chemistry  and  Toxicology.  By  JAMES 
W.  HOLLAND,  M.  D.,  Professor  of  Medical  Chemistry  and  Toxicology, 
and  Dean,  Jefferson  Medical  College,  Philadelphia.  Octavo  of  675 
pages,  fully  illustrated.  Cloth,  $3.00  net. 

THE  NEW  (3d)  EDITION 

Dr.  Holland's  work  is  an  entirely  new  one,  and  is  based  on  his  forty  years' 
practical  experience  in  teaching  chemistry  and  medicine.  It  has  been  subjected  to 
a  thorough  revision,  and  enlarged  to  the  extent  of  some  sixty  pages.  The  additions 
to  be  specially  noted  are  those  relating  to  the  electronic  theory',  chemical  equilib- 
rium, Kjeldahl's  method  for  determining  nitrogen,  chemistry  of  foods  and  their 
changes  in  the  body,  synthesis  of  proteins,  and  the  latest  improvements  in  urinary 
tests.  More  space  is  given  to  toxicology  than  in  any  other  text-book  on  chemistry. 

American  Medicine 

"  Its  statements  are  clear  and  terse  ;  its  illustrations  well  chosen  ;  its  development  logical, 
systematic,  and  comparatively  easy  to  follow.  .  .  .  We  heartily  commend  the  work." 

Ivy's  Applied  Anatomy  and 

Oral  Surgery  for  Dental  Students 


Applied   Anatomy  and   Oral   Surgery  for  Dental  Students.    By 

ROBERT  H.  IVY,  M.D.,  D.D.S.,  Assistant  Oral  Surgeon  to  the  Philadel- 
phia General  Hospital.     I2mo  of  280  pages,  illustrated.     Cloth,  $1.50 

net. 

FOR  DENTAL  STUDENTS 

This  work  is  just  what  dental  students  have  long  wanted — a  concise,  practical 
work  on  applied  anatomy  and  oral  surgery,  written  with  their  needs  solely  in 
mind.  No  one  could  be  better  fitted  for  this  task  than  Dr.  Ivy,  who  is  a  graduate 
in  both  dentistry  and  medicine.  Having  gone  through  the  dental  school,  he 
knows  precisely  the  dental  student's  needs  and  just  how  to  meet  them.  His 
medical  training  assures  you  that  his  anatomy  is  accurate  and  his  technic  modern. 
The  text  is  well  illustrated  with  pictures  that  you  will  find,  extremely  helpful. 

H.  P.  Kuhn,  M.D.,  Western  Dental  College,  Kansas  City. 

"  I  am  delighted  with  this  compact  little  treatise.     It  seems  to  me  just  to  fill  the  bill." 


CHEMISTRY,  SKIN,  AND   VENEREAL   DISEASES.  *3 

American  Pocket  Dictionary  New  (8th)  Edition 

THE  AMERICAN  POCKET  MEDICAL  DICTIONARY.  Edited  by  W.  A. 
NEWMAN  BORLAND,  M.  D.,  Editor  "  American  Illustrated  Medical 
Dictionary."  Containing  the  pronunciation  and  definition  of  the 
principal  words  used  in  medicine  and  kindred  sciences.  677  pages. 
Flexible  leather,  with  gold  edges,  $1.00  net;  with  thumb  index, 
#1.25  net. 
James  W.  Holland.  M.  D.. 

Professor  of  Medical  Chemistry  and  Toxicology,  and  Dean,  Jefferson  Medical  College 
Philadelphia, 

"  I  am  struck  at  once  with  admiration  at  the  compact  size  and  attractive  exterior.  ] 
can  recommend  it  to  our  students  without  reserve." 

Stelwagon's  Essentials  of  Skin  7th  Edition 

ESSENTIALS  OF  DISEASES  OF  THE  SKIN.  By  HENRY  W.  STEL- 
WAGON,  M.  D.,  PH.D.,  Professor  of  Dermatology  in  the  Jeffer- 
son Medical  College,  Philadelphia.  Post-octavo  of  291  pages, 
with  72  text-illustrations  and  8  plates.  Cloth,  $1.00  net.  In 
Saunders*  Question-  Compend  Series. 
The  Medical  News 

"  In  line  with  our  present  knowledge  of  diseases  of  the  skin.  .  .  .  Continues  to  main- 
tain the  high  standard  of  excellence  for  which  these  question  compends  have  been  noted." 

Wolffs  Medical  Chemistry  New  (7th)  Edition 

ESSENTIALS  OF  MEDICAL  CHEMISTRY,  ORGANIC  AND  INORGANIC. 
Containing  also  Questions  on  Medical  Physics,  Chemical  Physiol- 
ogy, Analytical  Processes,  Urinalysis,  and  Toxicology.  By  LAW- 
RENCE WOLFF,  M.  D.,  Late  Demonstrator  of  Chemistry,  Jefferson 
Medical  College.  Revised  by  A.  FERREE  WITMER,  PH.  G.,  M.  D., 
Formerly  Assistant  Demonstrator  of  Physiology,  University  of 
Pennsylvania.  Post-octavo  of  222  pages.  Cloth,  $1.00  net.  /« 
Saunders*  Question-  Compend  Series. 

Bliss*  Qualitative  Chemical  Analysis 

QUALITATIVE  CHEMICAL  ANALYSIS.  By  A.  R.  BLISS,  JR.,  PH.  G., 
M.  D.,  Professor  of  Chemistry  and  Pharmacy,  Birmingham 
Medical  College,  Alabama.  Octavo  of  250  pages.  Cloth,  $2.00 
net. 


Vecki's  Sexual  Impotence  New  (4th)  Edition 

SEXUAL  IMPOTENCE.  By  VICTOR  G.  VECKI,  M.  D.,  Consulting 
Genito-Urinary  Surgeon  to  Mt.  Zion  Hospital,  San  Francisco. 
I2mo  of  400  pages.  Cloth,  $2.25  net. 

Johns  Hopkins  Hospital  Bulletin 

"  A  scientific  treatise  upon  an  important  and  much  neglected  subject.  .  .  .  The 
treatment  of  impotence  in  general  and  of  sexual  neurasthenia  is  discriminating  and 
judicious." 


14  SAWDERS'   BOOKS  ON 


'   Chemical   Pathology 

Chemical  Pathology.  Being  a  discussion  of  General  Path- 
ology from  the  Standpoint  of  the  Chemical  Processes  Involved. 
By  H.  GIDEON  WELLS,  PH.  D.,  M.  D.,  Assistam  Professor  of 
Pathology  in  the  University  of  Chicago.  Octavo  of  616  pages. 
Cloth,  $3.25  net. 

Wm.   H.  Welch.  M.  D.,  Professor  of  Pathology,  Johns  Hopkins  University. 

"  The  work  fills  a  real  need  in  the  English  literature  of  a  very  important  subject,  and 
I  shall  be  glad  to  recommend  it  to  my  students." 


The  New  (2di   Edition 


Saxe's  Urinalysis 

Examination  of  the  Urine.  By  G.  A.  DE  SANTOS  SAXE,  M.  D., 
formerly  Instructor  in  Genito-Urinary  Surgery,  New  York  Post- 
graduate Medical  School  and  Hospital.  I2mo  of  448  pages,  fully 
illustrated.  Cloth,  $1.75  net. 

Francis  Carter  Wood,  M.  D.,    Adjunct  Professor  of  Clinical  Pathology,  Columbia   Uni- 
versity. 

"  It  seems  to  me  to  be  one  of  the  best  of  the  smaller  works  on  this  subject ;  it  is, 
indeed,  better  than  a  good  many  of  the  larger  ones." 

deSchweinitz  and  Randall  on  the  Eye,  Ear, 
Nose,  and  Throat 

American  Text-Book  of  Diseases  of  the  Eye,  Ear,  Nose,  and 
Throat.  Edited  by  G.  E.  DE  SCHWEINITZ,  M.D.,  and  B.  ALEX- 
ANDER RANDALL,  M.D.  Imperial  octavo,  1251  pages,  with  766 
illustrations,  59  of  them  in  colors.  Cloth,  $7.00  net;  Half  Mo- 
rocco, $8.50  net. 

Grunwald  and  Grayson  on  the  Larynx 

Atlas  and  Epitome  of  Diseases    of  the  Larynx.     By  Dr.  L. 

GRUNWALD,  of  Munich.  Edited,  with  additions,  by  CHARLES  P. 
GRAYSON,  M.D., /University  of  Pennsylvania.  With  107  colored 
figures  on  44  plates,  25  text-cuts,  and  103  pages  of  text.  Cloth, 
$2.50  net.  In  Saunders'  Hand- Atlas  Series. 

Mracek  and  Stelwagon's  Atlas  of  Skin         £££j! 

Atlas  and  Epitome  of  Diseases  of  the  Skin.  By  PROF.  DR. 
FRANZ  MRACEK,  of  Vienna.  Edited,  with  additions,  by  HENRY 
W.  STELWAGON,  M.D.,  Jefferson  Medical  College.  With  77  col- 
ored plates,  56  half-tone  illustrations,  and  280  pages  of  text.  In 
Saunters'  Hand-Atlas  Series.  Cloth,  $4.00  net. 


EYE,    EAR,    NOSE,   AND    THROAT.  15 

deSchweinitz    and    Holloway   on   Pulsating    Exoph- 
thalmos 

PULSATING  EXOPHTHALMOS.  An  analysis  of  sixty-nine  cases  not  pre- 
viously analyzed.  By  GEORGE  E.  DESCHWEINITZ,  M.  D.,  and  THOMAS 
B.  HOLLOWAY,  M.  D.  Octavo  of  125  pages.  Cloth,  $2.00  net. 

This  monograph  consists  of  an  analysis  of  sixty-nine  cases  of  this  affection 
not  previously  analyzed.  The  therapeutic  measures,  surgical  and  otherwise, 
which  have  been  employed  are  compared,  and  an  endeavor  has  been  made 
to  determine  from  these  analyses  which  procedures  seem  likely  to  prove  of 
the  greatest  value.  It  is  the  most  valuable  contribution  to  ophthalmic  liter- 
ature within  recent  years. 

British  Medical  Journal 

"  The  book  deals  very  thoroughly  with  the  whole  subject  and  in  it  the  most  complete  account  of 
the  disease  will  be  found." 

Jackson  on  the  Eye  The  New  (ad)  Edition 

A  MANUAL  OF  THE  DIAGNOSIS  AND  TREATMENT  OF  DISEASES  OF  THE 
EYE.  By  EDWARD  JACKSON,  A.  M.,  M.  D.,  Professor  of  Ophthalmology, 
University  of  Colorado.  i2mo  volume  of  615  pages,  with  184  beautiful 
illustrations.  Cloth,  $2.50  net. 


The  Medical  Record.  New  York 

.  .  .  _  Written  in  a  clear,  concise  manner,  it  bea 

appropriat 


"  It  is  truly  an  admirable  work.  .  .  .  Written  in  a  clear,  concise  manner,  it  bears  evidence  of  the 
author  s  comprehensive  grasp  of  the  subject.  The  term  '  multum  in  parvo '  is  an  appropriate  one  to 
apply  to  this  work." 


Grant  on   Face,   Mouth,   and  Jaws 

A  TEXT-BOOK  OF  THE  SURGICAL  PRINCIPLES  AND  SURGICAL  DISEASES 
OF  THE  FACE,  MOUTH,  AND  JAWS.  For  Dental  Students.  By  H.  HORACE 
GRANT,  A.  M.,  M.  D.,  Professor  of  Surgery  and  of  Clinical  Surgery, 
Hospital  College  of  Medicine,  Louisville.  Octavo  of  231  pages,  with 
68  illustrations.  Cloth,  $2.50  net. 

Preiswerk  and  Warren's  Dentistry 

ATLAS  AND  EPITOME  OF  DENTISTRY.  By  PROF.  G.  PREISWERK,  of 
Basil.  Edited,  with  additions,  by  GEORGE  W.  WARREN,  D.D.S.,  Pro- 
fessor of  Operative  Dentistry,  Pennsylvania  College  of  Dental  Surgery, 
Philadelphia.  With  44  lithographic  plates,  152  text-cuts,  and  343  pages 
of  text.  Cloth,  $3.50  net.  In  Sounders'  Atlas  Series. 

Asher's  Chemistry  and  Toxicology 

CHEMISTRY  AND  TOXICOLOGY  FOR  NURSES.  By  PHILIP  ASHER,  Pn.G., 
M.  D.,  Dean  and  Professor  of  Chemistry,  New  Orleans  College  of  Phar- 
macy. i2mo  of  190  pages.  Cloth,  $1.25  net. 


1 6  SAUNDERS'  BOOK'S  ON 

Wolfs  Examination  of  Urine 

A  LABORATORY  HANDBOOK  OF  PHYSIOLOGIC  CHEMISTRY  AND 
URINE-EXAMINATION.  By  CHARLES  G.  L.  WOLF,  M.  D.,  Instructor  in 
Physiologic  Chemistry,  Cornell  University  Medical  College,  New 
York.  1 2mo  volume  of  204  pages,  fully  illustrated.  Cloth,  $1.25  net. 

British  Medical  Journal 

"  The  methods  of  examining  the  urine  are  very  fully  described,  and  there  are  at  the 
end  of  the  book  some  extensive  tables  drawn  up  to  assist  in  urinary  diagnosis." 

Jackson's  Essentials  of  Eye  Third  Revised  Edition 

ESSENTIALS  OF  REFRACTION  AND  OF  DISEASES  OF  THE  EYE.  By 
EDWARD  JACKSON,  A.  M.,  M.  D.,  Emeritus  Professor  of  Diseases  of 
the  Eye,  Philadelphia  Polyclinic.  Post-octavo  of  261  pages,  82  illus- 
trations. Cloth,  $1.00  net.  In  Saunders1  Question- Compend  Series. 

Johns  Hopkins  Hospital  Bulletin 

"  The  entire  ground  is  covered,  and  the  points  that  most  need  careful  elucidation 
are  made  clear  and  easy." 

Gleason's  Nose  and  Throat  Fourth  Edition,  Revised 

ESSENTIALS  OF  DISEASES  OF  THE  NOSE  AND  THROAT.  By  E.  B. 
GLEASON,  S.  B.,  M.  D.,  Clinical  Professor  of  Otology,  Medico- 
Chirurgical  College,  Philadelphia,  etc.  Post-octavo,  241  pages,  1 12 
illustrations.  Cloth,  $1.00  net.  ///  Saunders'  Question  Compends. 
The  Lancet,  London 

"  The  careful  description  which  is  given  of  the  various  procedures  would  be  sufficient 
to  enable  most  people  of  average  intelligence  and  of  slight  anatomical  knowledge  to 
make  a  very  good  attempt  at  laryngoscopy." 

Gleason's  Diseases  of  the  Ear  Third  Edition,  Revised 

ESSENTIALS  OF  DISEASES  OF  THE  EAR.  By  E.  B.  GLEASON,  S.  B., 
M.  D.,  Clinical  Professor  of  Otology,  Medico-Chirurgical  College, 
Phila.,  etc.  Post-octavo  volume  of  214  pages,  with  114  illustra- 
tions. Cloth,  $  i  .00  net.  In  Sounders' Question- Compend  Series. 

Bristol  Medico-Chirurgical  Journal 

"  We  know  of  no  other  small  work  on  ear  diseases  to  compare  with  this,  either  in 
freshness  of  style  or  completeness  of  information." 

Wilcox  on  Genito- Urinary  and  Venereal  Diseases 

The  New  (2d)  Edition 

ESSENTIALS  OF  GENITO-URINARY  AND  VENEREAL  DISEASES.  By 
STARLING  S.  WILCOX,  M.  D.,  Lecturer  on  Genito-Urinary  Diseases 
and  Syphilology,  Starling-Ohio  Medical  College,  Columbus.  121110 
of  321  pages,  illustrated.  Cloth,  $1.00  net.  Saunders'  Commends. 

Stevenson's  Photoscopy 

PHOTOSCOPY  (Skiascopy  or  Retinoscopy).  By  MARK  D.  STEV- 
ENSON, M.  D.,  Ophthalmic  Surgeon  to  the  Akron  City  Hospital. 
I2mo  of  126  pages,  illustrated.  Cloth,  $1.25  net. 

Edward  Jackson.   M.  D.,  University  of  Colorado. 

"  It  is  well  written  and  will  prove  a  valuable  help.  Your  treatment  of  the  emergent 
pencil  of  rays,  and  the  part  falling  on  the  examiner's  eye,  is  decidedly  better  than  any 
previous  account." 


2  WKS  FROM  RECEIP 

UCSO 
MAR  0  .9  1992 


THE  LIBRARY 
UNIVERSITY  OF  C  YLIFORNIA 

LOS  ANGELES 


Biomedical 
Librvy 

WB 
200 

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°°0345788 


